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Berntt
22.09.2008, 18:28
Hallo,

man hat mir als individuellen Therapieversuch Somatostatin-Analoga ( konkret Lanoretide in der Dosierung 60mg 1x pro Monat) . Hat jemand von Euch mit dieser Therapie Erfahrung ?

Gruss Berntt

Harro
22.09.2008, 20:06
Gefunden

Hallo, Berntt, zu Lanreotide (http://nuklearmedizin.i-med.ac.at/dokumente/PatInfoLu177Lanreotide.pdf/view)

und hier (http://www.med.uni-marburg.de/stpg/ukm/lb/gastroendokrinol/studsek/studtherapie.htm)

zu Somatostatin (http://www.klinikum.uni-heidelberg.de/Somatostatin-Rezeptor-Szintigraphie.389.0.html)

Siehe auch hier (http://flexikon.doccheck.com/Somatostatin)

"Ein Idealist muss nicht dumm sein, aber enttäuscht wird er immer sein"
(Oscar Wilde)

Gruß Hutschi

BurgerH
23.09.2008, 07:59
Hallo Bernt,

hier findest Du eine Phase II Studie mit Somatostatin:

http://www.studien.de/includes/studien_ausgabe/studien_ausgabe.php?STUDIEN_ID=511

Sollte der Link nicht funktionieren, unter www.studien.de und dem Studien-ID 511 geht der Zugang auch.

Gruß

Hansjörg Burger.
Selbsthilfegruppe Prostatakrebs Rhein-Neckar e.V

JochenM
24.09.2008, 11:11
Hallo Berntt,
mich würde interessieren, wo Du eine solche Behandlung erhalten sollst? Muß Du diese selber zahlen oder findet dies im Rahmen einer Studie statt?
Für kurze Details wäre ich dankbar.
Viele Gruesse
Petra

WinfriedW
24.09.2008, 15:08
Hallo Berntt,
mich würde interessieren, wo Du eine solche Behandlung erhalten sollst? Muß Du diese selber zahlen oder findet dies im Rahmen einer Studie statt?
Für kurze Details wäre ich dankbar.
Viele Gruesse
PetraMich auch !!

WW

Berntt
24.09.2008, 15:35
Hallo,

die Anwendung von Somatostatin bei mir wurde in der Med. Hochschule Hannover Urologie zur Diskussion gestellt aufgrund der neuroendokrinen Differenzierung. Die Anwendung wäre ein individueller Therapieversuch, also keine Studie. . Die Kosten muss ich selbst übernehmen, ob ich die Kosten von der Krankenkversicherung ( privatversichert ) erstattet bekomme ( off label use) weiss ich nicht.

Man sollte bei Somatostatinanwendung keinen Blutzucker, keine Gallensteine und keine Pankreatitis haben.

Gruss Berntt

Hans-Joachim
24.09.2008, 16:46
Hallo Berntt, et.al.,

auch meine Onkologin trägt sich mit dem Gedanken, mir Octreotid zu verabreichen. Einen Kostenübernahmeantrag hat sie bei meiner (privaten) KK eingereicht und auch bewilligt bekommen.

Nach meinen Recherchen läuft diesbezüglich eine Studie in Hannover:
www.studien.de/includes/studien_ausgabe/studien_ausgabe.php?STUDIEN_ID=511 (http://www.studien.de/includes/studien_ausgabe/studien_ausgabe.php?STUDIEN_ID=511) und auch die Uni Marburg scheint sich hierzulande damit zu beschäftigen:
www.med.uni-marburg.de/stpg/ukm/lb/gastroendokrinol/studsek/studtherapie.htm (http://www.med.uni-marburg.de/stpg/ukm/lb/gastroendokrinol/studsek/studtherapie.htm)

Das Behandlungprotokoll scheint auf Koutsilieris zurückzugehen, der 2001 eine kleine Studie veröffentlicht hat, bei der 10 von 11 Patienten erfreulich angesprochen haben:

Department of Experimental Physiology, Medical School, University of Athens, Athens, 11527 Greece. mkouts@medscape.com
We evaluated whether the combination of triptorelin, a LHRH analog (LHRH-A), with dexamethasone and lanreotide, a somatostatin analog, can produce objective clinical responses in metastatic androgen ablation-refractory prostate cancer (stage D3) patients who have relapsed, after combined androgen blockade (LHRH-A plus antiandrogen) and antiandrogen withdrawal. Eleven stage D3 patients with diffuse bony metastases, who had progressed despite initial responses (lasting <12 months) to combined androgen blockade therapy and subsequently failed antiandrogen withdrawal, received oral dexamethasone (4 mg daily for the first month, tapered down to 2 mg after the first month and 1 mg after the second month, and continued on 1 mg thereafter) and lanreotide (30 mg im every 14 d) in combination with triptorelin (3.75 mg im every 28 d). Serum prostate-specific antigen, alkaline phosphatase, performance status, and bone pain were assessed monthly during therapy. Fasting blood glucose was measured biweekly, and serum IGF-I, T, and dehydroepiandrosterone sulfate levels were assessed at baseline, at response to the combination therapy, and at relapse from it. Ten of 11 stage D3 patients [90.9% of patients; 95% confidence interval (CI), 58.7-99.8%] had durable objective clinical responses (including > or = 50% prostate-specific antigen decline in 8 patients, 72.7%; 95% CI, 39-94%). All patients reported significant and durable improvement of bone pain (for a median duration of 13 months; 95% CI, 12-14 months; range, 6-22 months) and performance status (median duration, 19 months; 95% CI, 13-25 months; range, 7-22 months) without major treatment-related side effects. The median progression-free survival was 7 months (95% CI, 4-10 months; range, 3-17 months), and the median overall survival was 18 months (95% CI, 16-20 months; range, 7-22 months). Five of six total deaths occurred secondary to disease progression. We observed a statistically significant (P = 0.018) reduction in serum IGF-I levels at response to the combination therapy (60% reduction of baseline IGF-I levels). Dehydroepiandrosterone sulfate levels, although already significantly suppressed at baseline, had an additional significant reduction (P < 0.02) at response to therapy. T levels remained suppressed within castration levels (<3 nmol/liter, at baseline and throughout therapy, including relapse). The combination therapy of LHRH-A with dexamethasone plus somatostatin analog produces objective clinical responses and symptomatic improvement in androgen ablation (LHRH-A) refractory prostate cancer patients.
PMID: 11739429 [PubMed - indexed for MEDLINE]

Im Jahre 2004 hat er eine zweite Studie veröffentlicht, diesmal mit 38 Patienten, mit ähnlichem Ergebnis:

Combination of somatostatin analog, dexamethasone, and standard androgen ablation therapy in stage D3 prostate cancer patients with bone metastases.

<!--AuthorList-->Koutsilieris M (http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=Search&Term=%22Koutsilieris%20M%22%5BAuthor%5D&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_DiscoveryPanel.Pubmed_RVAbstractPlus), Mitsiades CS (http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=Search&Term=%22Mitsiades%20CS%22%5BAuthor%5D&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_DiscoveryPanel.Pubmed_RVAbstractPlus), Bogdanos J (http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=Search&Term=%22Bogdanos%20J%22%5BAuthor%5D&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_DiscoveryPanel.Pubmed_RVAbstractPlus), Dimopoulos T (http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=Search&Term=%22Dimopoulos%20T%22%5BAuthor%5D&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_DiscoveryPanel.Pubmed_RVAbstractPlus), Karamanolakis D (http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=Search&Term=%22Karamanolakis%20D%22%5BAuthor%5D&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_DiscoveryPanel.Pubmed_RVAbstractPlus), Milathianakis C (http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=Search&Term=%22Milathianakis%20C%22%5BAuthor%5D&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_DiscoveryPanel.Pubmed_RVAbstractPlus), Tsintavis A (http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=Search&Term=%22Tsintavis%20A%22%5BAuthor%5D&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_DiscoveryPanel.Pubmed_RVAbstractPlus).
Department of Experimental Physiology, Medical School, University of Athens, Goudi-Athens, Greece. mitsiades@dfci.harvard.edu
PURPOSE: Androgen ablation-refractory prostate cancer patients (stage D3) develop painful bone metastases and limited responsiveness to conventional therapies, hence the lack of universally accepted "gold standard" treatment for this poor prognosis clinical setting. We tested the safety and efficacy in stage D3 patients of the combination hormonal therapy, which combines administration of somatostatin analog and dexamethasone with standard androgen ablation monotherapy (luteinizing-hormone releasing-hormone analog or orchiectomy). EXPERIMENTAL DESIGN: Thirty eight patients with stage D3 prostate cancer (mean age 71.8 +/- 5.9 years) continued receiving androgen ablation therapy in combination with oral dexamethasone (4 mg daily for the 1st month of treatment, tapered down to 1 mg daily by the 4th month, with 1 mg daily maintenance dose thereafter) and somatostatin analog (20 mg octreotide i.m. injections every 28 days). RESULTS: Twenty-three of 38 patients (60.5%) receiving this combination regimen had partial responses [PR, >/=50% prostate-specific antigen (PSA) decline], 9 (21.1%) had stable disease, and 7 (18.4%) had progressive disease. In 47.7% (18 of 38) of patients, their serum PSA levels decreased with treatment but did not return to their respective baselines until the end of follow-up (or death from non-prostate cancer-related causes). The median time-to-return to baseline PSA was 12 months (95% CI, 7-17 months), median progression-free survival was 7 months (95% CI, 4.5-9.5 months), median overall survival was 14 months (95% CI, 10.7-17.4 months), and median prostate cancer-specific overall survival (defined as time from onset of combination therapy until prostate cancer-related death) was 16.0 months (95% CI, 11.9-20.1 months). All patients reported significant and durable improvement of bone pain and performance status (for a median duration of 14 months; 95% CI, 9-19 months), without major treatment-related side effects. We observed a statistically significant (P < 0.01) reduction in serum insulin-like growth factor-1 levels at response to the combination therapy. T levels remained suppressed within castration levels at baseline and throughout therapy, including relapse. CONCLUSION: The combination therapy of dexamethasone plus somatostatin analog and standard androgen ablation manipulation produces objective clinical responses and symptomatic improvement in androgen ablation-refractory refractory prostate cancer patients.
PMID: 15240528 [PubMed - indexed for MEDLINE]

Seine letzte, mir bekannte diesbezügliche Veröffentlichung stammt von 2006:

Combination therapy using LHRH and somatostatin analogues plus dexamethasone in androgen ablation refractory prostate cancer patients with bone involvement: a bench to bedside approach.

<!--AuthorList-->Koutsilieris M (http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=Search&Term=%22Koutsilieris%20M%22%5BAuthor%5D&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_DiscoveryPanel.Pubmed_RVAbstractPlus), Bogdanos J (http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=Search&Term=%22Bogdanos%20J%22%5BAuthor%5D&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_DiscoveryPanel.Pubmed_RVAbstractPlus), Milathianakis C (http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=Search&Term=%22Milathianakis%20C%22%5BAuthor%5D&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_DiscoveryPanel.Pubmed_RVAbstractPlus), Dimopoulos P (http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=Search&Term=%22Dimopoulos%20P%22%5BAuthor%5D&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_DiscoveryPanel.Pubmed_RVAbstractPlus), Dimopoulos T (http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=Search&Term=%22Dimopoulos%20T%22%5BAuthor%5D&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_DiscoveryPanel.Pubmed_RVAbstractPlus), Karamanolakis D (http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=Search&Term=%22Karamanolakis%20D%22%5BAuthor%5D&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_DiscoveryPanel.Pubmed_RVAbstractPlus), Halapas A (http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=Search&Term=%22Halapas%20A%22%5BAuthor%5D&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_DiscoveryPanel.Pubmed_RVAbstractPlus), Tenta R (http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=Search&Term=%22Tenta%20R%22%5BAuthor%5D&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_DiscoveryPanel.Pubmed_RVAbstractPlus), Katopodis H (http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=Search&Term=%22Katopodis%20H%22%5BAuthor%5D&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_DiscoveryPanel.Pubmed_RVAbstractPlus), Papageorgiou E (http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=Search&Term=%22Papageorgiou%20E%22%5BAuthor%5D&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_DiscoveryPanel.Pubmed_RVAbstractPlus), Pitulis N (http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=Search&Term=%22Pitulis%20N%22%5BAuthor%5D&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_DiscoveryPanel.Pubmed_RVAbstractPlus), Pissimissis N (http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=Search&Term=%22Pissimissis%20N%22%5BAuthor%5D&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_DiscoveryPanel.Pubmed_RVAbstractPlus), Lembessis P (http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=Search&Term=%22Lembessis%20P%22%5BAuthor%5D&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_DiscoveryPanel.Pubmed_RVAbstractPlus), Sourla A (http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=Search&Term=%22Sourla%20A%22%5BAuthor%5D&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_DiscoveryPanel.Pubmed_RVAbstractPlus).
University of Athens, Department of Basic Sciences, Medical School, 75 Micras Asias, Goudi-Athens 11527, Greece. mkouts@medscape.com
The development of resistance to anticancer therapies is a major hurdle in preventing long-lasting clinical responses to conventional therapies in hormone-refractory prostate cancer. Herein, the molecular evidence documenting that bone metastasis microenvironment survival factors (mainly the paracrine growth hormone-independent, urokinase-type plasminogen activator-mediated increase of IGF-1 and the endocrine production of growth hormone-dependent IGF-1, mainly liver-derived IGF-1 production) produce an epigenetic form of prostate cancer cells that are resistant to proapoptotic therapies is reviewed. Consequently, the authors present the conceptual framework of a novel antibone microenvironment survival factor, mainly an anti-IGF-1 hormonal manipulation for androgen ablation refractory prostate cancer (a combination of conventional androgen ablation therapy [luteinising hormone-releasing hormone agonist-A or orchiectomy]) with dexamethasone plus somatostatin analogue, which yielded durable objective responses and major improvement of bone pain and performance status in stage D3 prostate cancer patients.
PMID: 16787142 [PubMed - indexed for MEDLINE]

Dimopoulos hat 2006 eine vergleichende Studie zwischen Estramustin und Somatostatin durchgeführt, die in allen wesentlichen Parametern, keine signifikanten Unterschiede erbracht hat:

Combination of LHRH analog with somatostatin analog and dexamethasone versus chemotherapy in hormone-refractory prostate cancer: a randomized phase II study.

<!--AuthorList-->Dimopoulos MA (http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=Search&Term=%22Dimopoulos%20MA%22%5BAuthor%5D&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_DiscoveryPanel.Pubmed_RVAbstractPlus), Kiamouris C (http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=Search&Term=%22Kiamouris%20C%22%5BAuthor%5D&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_DiscoveryPanel.Pubmed_RVAbstractPlus), Gika D (http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=Search&Term=%22Gika%20D%22%5BAuthor%5D&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_DiscoveryPanel.Pubmed_RVAbstractPlus), Deliveliotis C (http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=Search&Term=%22Deliveliotis%20C%22%5BAuthor%5D&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_DiscoveryPanel.Pubmed_RVAbstractPlus), Giannopoulos A (http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=Search&Term=%22Giannopoulos%20A%22%5BAuthor%5D&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_DiscoveryPanel.Pubmed_RVAbstractPlus), Zervas A (http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=Search&Term=%22Zervas%20A%22%5BAuthor%5D&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_DiscoveryPanel.Pubmed_RVAbstractPlus), Alamanis C (http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=Search&Term=%22Alamanis%20C%22%5BAuthor%5D&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_DiscoveryPanel.Pubmed_RVAbstractPlus), Constantinidis C (http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=Search&Term=%22Constantinidis%20C%22%5BAuthor%5D&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_DiscoveryPanel.Pubmed_RVAbstractPlus), Koutsilieris M (http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=Search&Term=%22Koutsilieris%20M%22%5BAuthor%5D&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_DiscoveryPanel.Pubmed_RVAbstractPlus).
Department of Clinical Therapeutics, University of Athens School of Medicine, Athens, Greece.
OBJECTIVES: To evaluate prospectively the combination of a luteinizing hormone-releasing hormone analog with a somatostatin analog and dexamethasone in patients with hormone-refractory prostate cancer (HRPC) in a randomized Phase II study. HRPC presents a challenging therapeutic problem. Salvage chemotherapy is the usual approach at this stage of the disease. The combination of a luteinizing hormone-releasing hormone analog with a somatostatin analog and dexamethasone has produced objective clinical responses in HRPC. METHODS: Forty patients with HRPC were randomized to receive one of two treatments. Group 1 underwent chemotherapy (estramustine 140 mg three times daily and etoposide 100 mg orally for 21 days) and group 2 the combination of a somatostatin analog (lanreotide 30 mg intramuscularly every 14 days) and dexamethasone (4 mg tapered to 1 mg), in addition to androgen ablation by orchiectomy or a luteinizing hormone-releasing hormone analog (triptorelin 3.75 mg intramuscularly every 28 days). The clinical and prostate-specific antigen (PSA) response, overall survival, time to progression, and toxicity were compared between the two groups. RESULTS: The data of 20 patients in group 1 and 18 in group 2 were analyzed. The demographic and clinical data were similar in the two groups at study entry. A PSA response (decrease of greater than 50%) was observed in 45% of group 1 and 44% of group 2. The difference was not statistically significant. A partial clinical response was observed in 29% and 30% of groups 1 and 2, respectively. Again, the difference was not statistically significant. Changes in performance status and pain score during treatment were not significantly different in the two groups. Hematologic toxicity was more frequent in group 1 (80% of patients), and mild diabetes was more frequent in group 2 (22% of patients). The overall survival was 18.8 months in group 1 and 18 months in group 2 (not statistically significant). The time to progression was 6 versus 4 months and, in the PSA responder subgroup, it was 8 versus 7.7 months in groups 1 and 2, respectively (neither difference was statistically significant). CONCLUSIONS: The results of our randomized Phase II study indicated that the new combination treatment (luteinizing hormone-releasing hormone analog, somatostatin analog, and dexamethasone) may be equally effective as salvage chemotherapy in patients with HRPC in terms of the clinical and PSA response, overall survival, and time to progression. A larger prospective Phase III trial is required to confirm our observations.
PMID: 14751362 [PubMed - indexed for MEDLINE]

Berruti hat 2001 eine Studie durchgeführt, bei der der PSA nicht auf die Lanrotid-Gabe reagiert hat:

Effects of the somatostatin analog lanreotide on the circulating levels of chromogranin-A, prostate-specific antigen, and insulin-like growth factor-1 in advanced prostate cancer patients.

<!--AuthorList-->Berruti A (http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=Search&Term=%22Berruti%20A%22%5BAuthor%5D&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_DiscoveryPanel.Pubmed_RVAbstractPlus), Dogliotti L (http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=Search&Term=%22Dogliotti%20L%22%5BAuthor%5D&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_DiscoveryPanel.Pubmed_RVAbstractPlus), Mosca A (http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=Search&Term=%22Mosca%20A%22%5BAuthor%5D&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_DiscoveryPanel.Pubmed_RVAbstractPlus), Tarabuzzi R (http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=Search&Term=%22Tarabuzzi%20R%22%5BAuthor%5D&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_DiscoveryPanel.Pubmed_RVAbstractPlus), Torta M (http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=Search&Term=%22Torta%20M%22%5BAuthor%5D&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_DiscoveryPanel.Pubmed_RVAbstractPlus), Mari M (http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=Search&Term=%22Mari%20M%22%5BAuthor%5D&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_DiscoveryPanel.Pubmed_RVAbstractPlus), Gorzegno G (http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=Search&Term=%22Gorzegno%20G%22%5BAuthor%5D&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_DiscoveryPanel.Pubmed_RVAbstractPlus), Fontana D (http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=Search&Term=%22Fontana%20D%22%5BAuthor%5D&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_DiscoveryPanel.Pubmed_RVAbstractPlus), Angeli A (http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=Search&Term=%22Angeli%20A%22%5BAuthor%5D&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_DiscoveryPanel.Pubmed_RVAbstractPlus).
Dipartimento di Scienze Cliniche e Biologiche, Università di Torino, Oncologia Medica, Azienda Ospedaliera San Luigi, Orbassano (Torino), Italy.
BACKGROUND: The concept that neuroendocrine cells detected within prostate adenocarcinoma produce paracrine factors, that may exert a proliferative effect on exocrine prostate tumor cells, provides a rationale for the use of somatostatin analogs with the aim to counteract or delay the tumor progression. This study was designed to provide preliminary information on the effect of the administration of a long-acting somatostatin analog, lanreotide, on plasma levels of chromogranin A (CgA). Secondary aims were the evaluation of changes in circulating prostate-specific antigen (PSA) and insulin-like growth factor-1 (IGF-1). METHODS: Lanreotide (Ipstyl 30 mg; Ipsen, Milan, Italy) was administered intramuscularly every 14 days for 2 months to nine heavily pretreated prostate cancer patients with hormone refractory disease. All patients had, at baseline conditions, CgA values above the normal range. Androgen deprivation was maintained during the study period, while other concomitant antineoplastic treatments were not allowed. Serum PSA levels and plasma CgA and IGF-1 values were measured every week. RESULTS: Lanreotide treatment was very well tolerated and no patient experienced major toxicity. Plasma CgA values at baseline: mean 109 U/liter, standard deviation +/- 85 decreased significantly after treatment as follows: 42 U/liter, +/- 17.8; 27.2 U/liter +/- 13.6; 31.4 U/liter, +/- 17.8 and 27.6 U/liter, +/- 17.0; after 7, 14, 21, and 28 days, respectively (P < 0.01, Friedman ANOVA). Serum PSA did not change. Baseline IGF-1 was found to be above the detection limit in four cases, all of them showing a decrease after lanreotide. CONCLUSIONS: Lanreotide administration to prostate cancer patients induces a decrease in plasma CgA and IGF-1 levels, without any influence on serum PSA values. Prostate 47:205-211, 2001. Copyright 2001 Wiley-Liss, Inc.
PMID: 11351350 [PubMed - indexed for MEDLINE]

Mitsogiannis hat im März 2007 auf dem EAU-Kongress in Berlin folgende Studie mit 15 Patienten veröffentlicht, wobei er allerdings darauf hinweist, daß der PSA vor Beginn der Behandlung möglichst < 20 ng/ml sein sollte:

Mitsogiannis, I., Oeconomou, A., Gravas, S., Mitrakas, L., Tzortzis, V., Moutzouris, G., Melekos, M.

University of Thessaly, Urology, Larissa, Greece



Introduction & Objectives: Somatostatin analogues are deemed to have a favourable effect on metastatic prostate cancer. These agents prevent cell proliferation by inducing cell cycle arrest and apoptosis. These effects are believed to be mediated by specific receptors (SSTR) located on the tumour cells and also by receptors on non-tumour cell targets which inhibit the secretion of hormones and growth factors involved in promoting tumour cell growth, inhibiting angiogenesis, promoting vasoconstriction and modulating immune cell function. Somatostatin analogues combined with dexamethasone have previously been shown to produce objective clinical responses and symptomatic improvement in patients with HRPCA. The aim of this study was to assess the efficacy and safety of a somatostatin analogue (lanreotide 90 mg) in combination with dexamethasone in the treatment of patients with HRPCA.


Material & Methods: A total of 15 patients, aged 56-86 years (mean 74.1), were enrolled in the study. All had been diagnosed with HRPCA which was metastatic to the bones. The mean initial PSA value was 122.7 ng/ml (range 3-1035, median 33 ng/ml). Patients received lanreotide (Somatuline), 90 mg intramuscularly once a month, plus dexamethasone orally (4 mg daily for a month, reduced to half the dose every month until an ultimate dose of 0.5 mg daily), without discontinuing the LHRH analogue. Follow up included PSA measurements 1 month after initiation of treatment and every 3 months thereafter, bone scan every 6 months and assessment of the need for oral analgesia to control bone pain.


Results: Themean follow up period was 8.8 months (3-30). In 7 patients (46.7%) a >50% reduction of the PSA value was noticed from the first month of treatment, whereas 8 patients (53.3%) had progressive disease (steady elevation of PSA in 2 consecutive measurements). Of the 7 responders, 5 had complete response and 2 had partial response. The mean initial PSA in patients who responded was 28.5 ng/ml (range 3-92, median 13.7) and, furthermore, 5 of these patients had an initial PSA of <20 ng/ml. In contrast, in all the non-responders the baseline PSA was >20 ng/ml (mean 205.1; range 21-1035, median 82.3). Overall, the mean duration of response was 15.4 months (7-30). Three responders discontinued analgesics, whereas 4 reduced the required dose. In the 2 patients with partial response the disease finally progressed (7 and 12 months after initiation of therapy); in the remaining 5 (complete responders) the mean duration of response was 17.8 months (12-30). Treatment-related side effects were gastrointestinal disturbances in 4 patients, hyperglycaemia in a diabetic patient and transient elevation of serum creatinine level in 3 patients. No patient developed hepatic dysfunction.


Conclusions: The combination of lanreotide 90 mg plus dexamethasone may be of value in patients with HRPCA who have a low (<20 ng/ml) initial PSA and respond early to treatment.

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Liebe Mitstreiter,

vorerst eine Menge Stoff zum Lesen. Aber die Therapie scheint nicht uninteressant zu sein.

Was meint Ihr dazu? Wer weiß mehr dazu?

Gruß Joachim<!-- -->
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HansiB
24.09.2008, 17:50
Hallo Freunde,

die "Studie" soll wohl ein Witz sein, Ausschlusskriterien u. a. Metastasen. Wer kommt dafür überhaupt in Frage?

Gruß Konrad

JochenM
26.09.2008, 16:41
Lieber Konrad,
die gleiche Frage habe ich mir auch gestellt!?

Petra

poseidon
21.10.2008, 20:27
Hallo,
da sich bislang niemand zu Berntts Frage geäußert hat, möchte ich sie nochmal wiederholen.Gibt es jemand der bereits mit Somatostatin behandelt wird?

Berntt
22.10.2008, 21:49
Hallo,

ich habe vor ca. 3 Wochen 60mg Lanreotide erhalten. Nebenwirkungen: nur am 1. Tag starke Oberbauchschmerzen, sonst bisher kaum Nebenwirkungen. Gleichzeitig Einnahme von Dexamethason 4 mg tgl.

PSA ca. 10 Tage nach Anwendung von 4,3 auf 3,8 gesunken, CGA von 120 auf ca. 35 gesunken.

Ich werde später über den weiteren Verlauf berichten.

Gruss Berntt

weinreich
03.11.2008, 16:34
hallo

ein neuer artikel ist in der fachzeitschrift der urologe heft 10, 2008 seite 1334.. titel samatostatin-analoga in der therapie des hrpc.

www. der urologe.de

aus hbg

manni