Objective: To explore the feasibility, safety and clinical effect of mid-frequency transcutaneous electrical acupoint stimulation (TEAS) combined with oral tamoxifen (TAM) in the treatment of oligoasthenozoospermia. METHODS: We randomly and equally assigned 120 patients with idiopathic oligoasthenozoospermia to receive oral TAM, mid-frequency TEAS, or TAM+TEAS, all for 8 weeks. Before and after treatment, we recorded the semen volume, total sperm count, sperm concentration, sperm motility, percentage of progressively motile sperm (PMS), and the levels of follicle-stimulating hormone (FSH), luteotrophic hormone (LH) and testosterone (T) in the peripheral serum and compared these parameters among the three groups of patients. RESULTS: Compared with the baseline, none of the patients showed significant improvement in the semen volume (P >0.05) but all exhibited remarkably elevated levels of serum FSH, LH and T after treatment (P <0.05); TAM significantly improved the total sperm count (［25.16 ± 2.05］ vs ［42.65 ± 5.78］ ×106, P <0.05) and sperm concentration (［12.15 ± 2.51］ vs ［24.31 ± 2.59］ ×10⁶/ml, P <0.05), but not total sperm motility (［21.78 ± 8.81］ vs ［22.61 ± 5.75］ %, P >0.05) or PMS (［15.87 ± 7.81］ vs ［16.76 ± 5.86］ %, P >0.05); TEAS markedly increased total sperm motility (［24.81 ± 8.27］ vs ［32.43 ± 4.97］ %, P <0.05) and PMS (［19.71 ± 9.15］ vs ［27.17 ± 5.09］%, P <0.05), but not the total sperm count (［23.23 ± 3.14］ vs ［25.87 ± 4.96］ ×106, P >0.05) or sperm concentration (［11.27 ± 2.24］ vs ［14.12 ± 2.47］ ×10⁶/ml, P >0.05); TAM+TEAS, however, improved not only the total sperm count (［26.17 ± 5.05］ vs ［ 51.14 ± 3.69］×106, P <0.05) and sperm concentration (［12.78 ± 2.41］ vs ［27.28 ± 1.98］ ×10⁶/ml, P <0.05), but also total sperm motility (［23.89 ± 9.05］ vs ［37.12 ± 5.33］%, P <0.05) and PMS (［17.14 ± 8.04］ vs ［31.09 ± 7.12］%, P <0.05). The total effectiveness rate was significantly higher in the TAM+TEAS group than in the TAM and TEAS groups (97.5% vs 72.5% and 75.0%, P <0.05). CONCLUSIONS Mid-frequency TEAS combined with tamoxifen can significantly improve semen quality and increase sex hormone levels in patients with idiopathic oligoasthenozoospermia.
Acupuncture Points ; Antineoplastic Agents, Hormonal ; administration & dosage ; therapeutic use ; Asthenozoospermia ; blood ; therapy ; Combined Modality Therapy ; methods ; Electroacupuncture ; methods ; Feasibility Studies ; Follicle Stimulating Hormone ; blood ; Humans ; Male ; Oligospermia ; blood ; therapy ; Prolactin ; blood ; Semen Analysis ; Sperm Count ; Sperm Motility ; Tamoxifen ; administration & dosage ; therapeutic use ; Testosterone ; blood

Objective: To investigate the clinical effects of integrated traditional Chinese and Western medicine in the treatment of castration-resistant prostate cancer (CRPC). METHODS: A total of 54 CRPC patients were randomly divided into a control and a trial group, all treated by endocrine therapy (oral Bicalutamide at 50 mg per d plus subcutaneous injection of Goserelin at 3.6 mg once every 4 wk) and chemotherapy (intravenous injection of Docetaxel at 75 mg/m2 once every 3 wk plus oral Prednisone at 5 mg bid), while the latter group by Fuyang Huayu Prescription (a Traditional Chinese Medicine ［TCM］ prescription for tonifying yang and dispersing blood stasis) in addition, for a course of 24 weeks. Comparisons were made between the two groups of patients in the level of serum prostate-specific antigen (PSA), Karnofsky physical condition scores, function assessment of cancer therapy-prostate (FACT-P) scores, and TCM symptoms scores before and after 12 or 24 weeks of treatment. RESULTS: Compared with the baseline, the serum PSA level was significantly decreased after 12 weeks of treatment both in the control (［25.9 ± 39.3］ vs ［20.0 ± 21.1］ μg/L, P <0.05) and in the trial group (［22.1 ± 33.9］ vs ［17.9 ± 19.1］ μg/L, P <0.05), with no statistically significant differences between the two groups (P >0.05). At 24 weeks, however, the PSA levels in the control and trial groups were slightly increased to (23.1 ± 28.4) and (19.6 ± 23.5) μg/L, respectively, with no statistically significant differences in between (P >0.05). Karnofsky, FACT-P and TCM symptoms scores were all markedly improved in the trial group after 12 weeks of treatment (P <0.05) and remained stable at 24 weeks, but not in the control group either at 12 or at 24 weeks (P >0.05). CONCLUSIONS TCM Fuyang Huayu Prescription combined with endocrine therapy and chemotherapy is effective for CRPC.
Anilides ; administration & dosage ; Antineoplastic Agents, Hormonal ; therapeutic use ; Antineoplastic Combined Chemotherapy Protocols ; therapeutic use ; Docetaxel ; Drug Administration Schedule ; Goserelin ; administration & dosage ; Humans ; Male ; Nitriles ; administration & dosage ; Prednisone ; administration & dosage ; Prostate-Specific Antigen ; blood ; Prostatic Neoplasms, Castration-Resistant ; blood ; drug therapy ; Taxoids ; administration & dosage ; Tosyl Compounds ; administration & dosage ; Treatment Outcome

PURPOSE: To investigate the efficacy of androgen deprivation treatment (ADT) between continuous and intermittent ADT. MATERIALS AND METHODS: Between January 2006 and May 2015, 603 patients were selected and divided into continuous ADT (CADT) (n=175) and intermittent ADT (IADT) (n=428) groups. The median follow-up in this study was 48.19 (1.0-114.0) months. The primary end point was time to castration resistant prostate cancer (CRPC). The types of ADT were monotherapy and maximal androgen blockade (i.e., luteinizing hormone-releasing hormone agonist and antiandrogen). RESULTS: The characteristics of patients showed no significant differences between the CADT and IADT groups, except for the Gleason score (p<0.001). The median time to CRPC of all enrolled patients with ADT was 20.60±1.60 months. The median time to CRPC was 11.20±1.31 months in the CADT group as compared with 22.60±2.08 months in the IADT group. In multivariate analysis, percentage of positive core (p=0.047; hazard ratio [HR], 0.976; 95% confidence interval [CI], 0.953-1.000), Gleason score (p=0.007; HR, 1.977; 95% CI, 1.206-3.240), lymph node metastasis (p=0.030; HR, 0.498; 95% CI, 0.265-0.936), bone metastasis (p=0.028; HR, 1.921; 95% CI, 1.072-3.445), and CADT vs. IADT (p=0.003; HR, 0.254; 95% CI. 0.102-0.633) were correlated with the duration of progression to CRPC. The IADT group presented a significantly longer median time to CRPC compared with the CADT group. Additionally, patients in the IADT group showed a longer duration in median time to CRPC in subgroup analysis according to the Gleason score. CONCLUSIONS: This study found that IADT produces a longer duration in median time to CRPC than does CADT.
Adenocarcinoma/*drug therapy/pathology/secondary ; Aged ; Aged, 80 and over ; Androgen Antagonists/*administration & dosage/therapeutic use ; Antineoplastic Agents, Hormonal/*administration & dosage/therapeutic use ; Disease Progression ; Drug Administration Schedule ; Follow-Up Studies ; Humans ; Lymphatic Metastasis ; Male ; Middle Aged ; Neoplasm Grading ; Prostatic Neoplasms/*drug therapy/pathology ; Prostatic Neoplasms, Castration-Resistant/drug therapy/pathology ; Retrospective Studies ; Treatment Outcome

OBJECTIVETo search for an effective hormonal therapy for delaying the progression of prostate cancer to androgen-independent prostate cancer (AIPC).

METHODSThis study included 93 cases of prostate cancer confirmed by transrectal ultrasound-guided biopsy, 22 treated by bilateral orchiectomy plus bicalutamide as a continuous androgen deprivation (CAD) therapy, and the other 71 by the intermittent androgen deprivation (IAD) therapy, the latter divided into a standard IAD group (n = 29) and a modified IAD group (n = 42) to be treated by maximum androgen blockage (MAB) until the serum PSA level decreased to less than 0.2 microg/L and the medication was maintained for 3 months. Entering the intermittent period, the patients of the standard IAD group discontinued medication, while those in the modified IAD group withdrew luteinizing hormone-releasing hormone analogue (LHRH-a) but continued the use of bicalutamide. MAB was resumed in these two groups when serum PSA manifested a continuous rise and went up to 4 microg/L until prostate cancer progressed to AIPC. Comparisons were made among the CAD, standard IAD and modified IAD groups in the follow-up time, time of progression to CRPC and treatment cycles.

RESULTSThe three groups of patients were well balanced in terms of demographics, baseline characteristics and follow-up time. The median times of progression to AIPC in the CAD, standard IAD and modified IAD groups were (26.50 +/- 4.15), (30.00 +/- 7.83) and (34.93 +/- 5.08) months, respectively, with statistically significant differences between the modified IAD group and the CAD (P = 0.001) and standard IAD (P = 0.032), but not between the latter two groups (P = 0.143). Kaplan-Meier survival curves showed a significantly longer median time of progression to AIPC in the modified than in the standard IAD group (P = 0.01). The mean cycle length was (16.13 +/- 3.33) months for the standard IAD group and (19.58 +/- 4.30) months for the modified IAD group, and the time off treatment of the first cycle was (9.6 +/- 3.2) months in the former and (14.2 +/- 3.7) months in the latter, with significant difference between the two groups (P = 0.001).

CONCLUSIONCompared with CAD and standard IAD, modified IAD therapy can significantly prolong the time of progression to AIPC in patients with prostate cancer.

Aged ; Aged, 80 and over ; Androgen Antagonists ; administration & dosage ; therapeutic use ; Anilides ; administration & dosage ; therapeutic use ; Antineoplastic Agents, Hormonal ; administration & dosage ; therapeutic use ; Disease Progression ; Humans ; Male ; Middle Aged ; Nitriles ; administration & dosage ; therapeutic use ; Prognosis ; Prostatic Neoplasms ; diagnosis ; drug therapy ; Tosyl Compounds ; administration & dosage ; therapeutic use ; Treatment Outcome

OBJECTIVETo investigate the safety and medication cycles of intermittent androgen deprivation (IAD) in the treatment of aggressive prostate cancer.

METHODSBased on prostate cancer clinical staging, we divided 178 patients with aggressive prostate cancer into groups A (T3-4N0M0), B (TXN1M0) and C (TXNXM1) to receive maximum androgen blockage for at least 6 months till the PSA level remained at < or = 0.2 microg/L for 3 months, followed by an off-period (without medication). The on-period was initiated when the PSA level was > 4 microg/L, and then stopped again when it was < or = 0.2 microg/L. We recorded and compared the patients' age, baseline PSA levels, Gleason scores, duration of on- and off-period, and time to tumor progression.

RESULTSThe baseline PSA levels of the 3 groups were (27.5 +/- 14.6), (43.4 +/- 21.8) and (62.8 +/- 44.6) microg/L, P < 0.01; the follow-ups averaged (38.4 +/- 9.6), (33.1 +/-14.0) and (28.3 +/- 14.3) months; and the times from medication initiation to tumor progression were (37.4 +/- 6.6), (27.4 +/- 10.2) and (16.6 +/- 4.4) months, respectively. Group A showed a longer off-period and more medication cycles than B and C (P < 0.01). Nineteen patients completed 5 cycles and 2 died of cardiovascular events in group A. PSA elevation and cancer progression occurred after 3 cycles at most in group C. Six died in group B, 1 of metastatic prostate cancer, and 36 died in group C, 21 of metastasis.

CONCLUSIONFor local aggressive prostate cancer, IAD can effectively slow down tumor progression, reduce adverse events and improve patients' quality of life.

Aged ; Aged, 80 and over ; Androgen Antagonists ; administration & dosage ; therapeutic use ; Antineoplastic Agents, Hormonal ; administration & dosage ; therapeutic use ; Humans ; Male ; Middle Aged ; Prostatic Neoplasms ; drug therapy ; Treatment Outcome

OBJECTIVETo study the demethylation effect of arsenic trioxide (As2O3) on ERα-negative human breast cancer MDA-MB-435s cells and its possible mechanisms, and to observe its treatment efficacy in combination with tamoxifen (TAM) after ERα re-expression.

METHODSMTT assay was used to examine the inhibitory effect of As2O3 treatment alone or in combination with TAM on cell proliferation. A nude mouse xenograft model was used to further examine the treatment efficacy in vivo. MSP was used to detect the methylation status of ERα gene after treated with As2O3 in MDA-MB-435s cells and the transplanted tumor tissues. RT-PCR was used to detect the mRNA expression of DNMT1 and Erα. Western bolt was used to detect the DNMT1 and ERα protein expression. The diameter of xenograft tumors was measured weekly, and the tumor growth curve was drawn.

RESULTSThe level of proliferation of the MDA-MB-435s cells was significantly suppressed after treatment with different concentration of As2O3 alone or As2O3 combined with TAM, and the 4 µmol/L As2O3 + TAM treatment for 72 h showed the highest inhibition rate (62.6%). 1, 2, 4 µmol/L As2O3 had demethylation effect on MDA-MB-435s cells, and the DNMT1 mRNA and protein expression was inhibited and accompanied by ERα mRNA and protein re-expression. The unmethylation specific bands of ERα gene were enhanced after treated by As2O3 alone or As2O3 combined with TAM in the xenograft tumors. The expression of DNMT1 mRNA and protein was inhibited, and accompanied by ERα mRNA and protein re-expression. An significant decrease of volume and weight of the xenograft tumors in the As2O3 treated alone or combined with TAM groups was observed compared with those of the normal saline group or TAM alone group (P < 0.05), and the 4 mg/kg As2O3 + TAM group had the highest inhibition rate of tumor weight (79.5%) and volume (76.4%).

CONCLUSIONSERα can be re-expressed in ERα-negative breast cancer MDA-MB-435s cells after treated with As2O3 by inhibiting the DNMT1 activity. MDA-MB-435s cells are re-sensitized to endocrine therapy after ERα re-expression. As2O3 combined with TAM may provide a new therapeutic approach for patients with ERα-negative breast cancer in the clinic.

Animals ; Antineoplastic Agents ; administration & dosage ; pharmacology ; Antineoplastic Agents, Hormonal ; administration & dosage ; Antineoplastic Combined Chemotherapy Protocols ; pharmacology ; Arsenicals ; administration & dosage ; pharmacology ; Breast Neoplasms ; genetics ; metabolism ; pathology ; Cell Line, Tumor ; Cell Proliferation ; drug effects ; DNA (Cytosine-5-)-Methyltransferase 1 ; DNA (Cytosine-5-)-Methyltransferases ; DNA Methylation ; Dose-Response Relationship, Drug ; Estrogen Receptor alpha ; genetics ; metabolism ; Female ; Humans ; Mice ; Mice, Inbred BALB C ; Mice, Nude ; Oxides ; administration & dosage ; pharmacology ; RNA, Messenger ; metabolism ; Tamoxifen ; administration & dosage ; Tumor Burden ; drug effects ; Xenograft Model Antitumor Assays

BACKGROUNDAlthough previous clinical study revealed that bortezomib combined with dexamethasone had improved the outcomes of relapsed or refractory multiple myeloma (RRMM), the optimal dose combinations of bortezomib and dexamethasone remain unknown. This trial aimed to observe the efficacy and safety of different dose combinations of bortezomib and dexamethasone in the treatment of RRMM patients in China.

METHODSA total of 168 patients with relapsed multiple myeloma (MM) who were refractory to at lest two prior treatments were enrolled in this multicenter, open-label, non-randomized, prospective clinical trial. Twenty patients received 1.3 mg/m(2) of bortezomib twice weekly for 2 weeks of a 3-week cycle for up to 8 cycles and oral or intravenous dexamethasone 20 mg on the day of and after each bortezomib dose (group 1); 66 patients received less than 1.3 mg/m(2) (0.7 - 1.0 mg/m(2)) of bortezomib and dexamethasone 20 mg on the same schedule (group 2); 37 patients received 1.3 mg/m(2)2 of bortezomib and dexamethasone 40 mg (group 3) and 45 patients received less than 1.3 mg/m(2) (0.7 - 1.0 mg/m(2)) of bortezomib and dexamethasone 40 mg (group 4). The response was evaluated according to the criteria of the European Group for Blood and Marrow Transplantation and confirmed by an independent review committee. Adverse events were graded according to the National Cancer Institute Common Toxicity Criteria, version 3.0.

RESULTSThe median age of groups 1 to 4 was 61, 62, 56, and 60 years, respectively. Most patients were in stages II/III of MM and the most common subtype was IgG. The rate of overall response to bortezomib and dexamethasone of group 1 to 4 was 72.2% (13/18), 73.8% (48/65), 78.8% (26/33) and 78.0% (32/41) (P = 0.91), including a complete response rate of 22.2% (4/18), 20.0% (13/65), 33.3% (11/33) and 29.3% (12/41) (P = 0.67), respectively. There was no statistical significance in time to progression and overall survival among these 4 groups (P > 0.05). The most commonly adverse events of any grade in the entire 4 groups were fatigue, gastrointestinal effects, peripheral neuropathy and thrombocytopenia, and there was no significance in the number of adverse events among the 4 groups (P > 0.05) except that peripheral neuropathy was reported more frequently in group 3 (36.3%) than in group 2 (13.8%, P < 0.05) and group 4 (14.6%, P < 0.05).

CONCLUSIONSThe combination of bortezomib and dexamethasone was associated with high responses in Chinese RRMM patients. No significant differences of efficacy were detected in different dose combinations of bortezomib and dexamethasone. Moreover, low dose of bortezomib reduced the incidence of peripheral neuropathy without affecting outcome in the treatment of patients with RRMM in China.

Antineoplastic Agents ; administration & dosage ; Antineoplastic Agents, Hormonal ; administration & dosage ; Antineoplastic Combined Chemotherapy Protocols ; therapeutic use ; Boronic Acids ; administration & dosage ; Bortezomib ; China ; Dexamethasone ; administration & dosage ; Drug Therapy, Combination ; Female ; Humans ; Male ; Middle Aged ; Multiple Myeloma ; drug therapy ; Neoplasm Recurrence, Local ; Prospective Studies ; Pyrazines ; administration & dosage

OBJECTIVETo explore the regulation mechanism of the reversal of breast cancer resistance protein-mediated multidrug resistance by toremifene.

METHODSTwo recombinant plasmids (pcDNA3-promoter-BCRP and pcDNA3-CMV-BCRP) were designed to express the wild-type full-length BCRP cDNA enforced driven by its endogenous promoter containing a functional ERE and a CMV promoter as control, respectively. Two recombinant plasmids were transfected into ERα-positive MCF-7 and ERα-negative MDA-MB-231 breast cancer cell lines. Four kinds of BCRP expressing cell lines of MCF-7/Promoter-BCRP, MCF-7/CMV-BCRP, MDA-MB-231/Promoter-BCRP and MDA-MB-231/CMV-BCRP were established in which BCRP was promoted by the BCRP promoter and a CMV promoter as control, respectively. The drug resistant cells were treated with toremifene. Then RT-PCR, Western blot, mitoxantrone efflux assays and cytotoxicity assay were performed to detect the reversal function of BCRP by toremifene on the drug resistance cell lines.

RESULTSToremifene significantly downregulated BCRP mRNA levels in a dose-dependent manner in ERα-positive MCF-7/Promoter-BCRP cells than that of untreated control cells. In MCF-7/Promoter-BCRP cells, toremifene at the dose of 0.1, 1 and 10 µmol/L decreased BCRP mRNA expression by 29.5% (P < 0.05), 68.1% (P < 0.01) and 97.4% (P < 0.01), respectively. After being treated with toremifene and 17β-estradiol, the BCRP mRNA level in MCF-7/Promoter-BCRP cells was 64.2% ± 1.3%, significantly higher than that of toremifene treatment control cells (3.8% ± 0.2%,P < 0.01). Furthermore, the effect of toremifene on BCRP protein is similar in BCRP mRNA. Toremifene obviously increased the mitoxantrone fluorescence intensity and decreased the efflux activity by 47.3% (P < 0.05) in MCF-7/promoter-BCRP cells when compared with the untreated control, whereas intracellular accumulation of mitoxantrone obviously decreased and the efflux activity increased by 61.5% were observed in combination with 17β-estradiol when compared with toremifene treatment alone. The results therefore suggested that toremifene reversed mitoxantrone resistance in MCF-7/Promoter-BCRP cells. However, in MCF-7/CMV-BCRP, MDA-MB-231/Promoter-BCRP and MDA-MB-231/CMV-BCRP cells, toremifene or in combination with 17β-estradiol did not affect intracellular mitoxantrone uptake.

CONCLUSIONTaken together, our findings indicate that expression of BCRP is downregulated by toremifene, via a novel transcriptional mechanism which might be involved in the ERE of BCRP promoter through ER-mediated to inactivate the transcription of BCRP gene.

ATP Binding Cassette Transporter, Sub-Family G, Member 2 ; ATP-Binding Cassette Transporters ; genetics ; metabolism ; Antineoplastic Agents ; pharmacology ; Antineoplastic Agents, Hormonal ; administration & dosage ; pharmacology ; Breast Neoplasms ; genetics ; metabolism ; pathology ; Cell Line, Tumor ; Cytomegalovirus ; genetics ; Dose-Response Relationship, Drug ; Down-Regulation ; Drug Resistance, Multiple ; drug effects ; Drug Resistance, Neoplasm ; drug effects ; Estradiol ; pharmacology ; Estrogen Receptor alpha ; metabolism ; Female ; Gene Expression Regulation, Neoplastic ; Humans ; Mitoxantrone ; pharmacology ; Neoplasm Proteins ; genetics ; metabolism ; Plasmids ; Promoter Regions, Genetic ; RNA, Messenger ; metabolism ; Recombinant Proteins ; genetics ; metabolism ; Response Elements ; genetics ; Toremifene ; administration & dosage ; pharmacology

The increased survival of patients with breast cancer has given rise to other problems associated with the complications of chemotherapy. One major complication is premature ovarian failure, an especially harmful outcome for women of reproductive age. This study was performed to evaluate the efficacy of GnRH agonist (GnRHa) treatment on protecting ovarian function in young breast cancer patients (30.59+/-5.1 yr) receiving chemotherapy after surgery. Twenty-two women were enrolled and given subcutaneous injections of leuprolide acetate (3.75 mg) every 4 weeks during chemotherapy. Follow-up laboratory tests (luteinizing hormone [LH], follicle stimulating hormone [FSH], and estradiol) were performed 1, 3, and 6 months after chemotherapy. Menstruation patterns and clinical symptoms were followed up for a mean duration of 35.6+/-1.7 months. FSH and LH levels were normal in all patients 6 months after completing chemotherapy (8.0+/-5.3, 4.4+/-2.7 mIU/mL, respectively). During follow-up, none of the patients complained of menopausal symptoms and 81.8% experienced recovery of menstruation. This report is the first trial of GnRHa as a treatment modality to protect ovarian function during adjuvant chemotherapy in young Korean breast cancer patients.
Adult ; Antineoplastic Agents/adverse effects/therapeutic use ; Antineoplastic Agents, Hormonal/therapeutic use ; Breast Neoplasms/diagnosis/*drug therapy/surgery ; Combined Modality Therapy ; Cyclophosphamide/adverse effects/therapeutic use ; Doxorubicin/adverse effects/therapeutic use ; Female ; Follicle Stimulating Hormone/analysis ; Gonadotropin-Releasing Hormone/*agonists ; Humans ; Leuprolide/administration & dosage ; Luteinizing Hormone/analysis ; Menstruation ; Ovarian Function Tests ; Primary Ovarian Insufficiency/etiology/*prevention & control ; Republic of Korea ; Tamoxifen/therapeutic use ; Time Factors

OBJECTIVETo evaluate the efficacy and safety of gonadotropin-releasing hormone analogue (GnRHa) triptorelin 11.25 mg 3-month sustained release formulations in the treatment of metastatic prostate cancer.

METHODSFrom January 2004 to March 2006, a randomized, parallel-controlled, multicenter clinical trial was conducted. One hundred and twenty-seven patients with documented metastatic prostate cancer were randomized to receive one injection of the 11.25 mg formulation triptorelin (n = 65) or three injections at 28-day intervals of the 3.75 mg formulation (n = 62). Changes from baseline of TPSA, prostate volume, testosterone, LH, FSH, PRL and estradiol were assessed over 3 months. Changes of the metastatic lesions were also observed and evaluated. The occurrences of adverse events were evaluated as well.

RESULTSAfter 3 months treatment, total PSA level decreased significantly from baseline both in 11.25 mg group and 3.75 mg group. At 30, 60 and 90 days, TPSA (median level) declined from 164.55 microg/L into 11.34, 4.12, 3.89 microg/L in 11.25 mg group, and from 101.38 microg/L into 6.88, 2.41, 2.57 microg/L in control group respectively. The patients ratio with over 90% decreasing from TPSA baseline were 78.6% and 75.5% respectively in two groups (P = 0.700). Prostate volume were also decreased significantly in both groups, median volume declined from 48.0 mm(3) into 21.5 mm(3) in 11.25 mg group and from 45.0 mm(3) into 21.0 mm(3) in 3.75 mg group. No significant differences were found between the two groups in changes of TPSA (P = 0.601) and prostate volume (P > 0.05). Both formulations were able to induce castration levels, 0.31 microg/L in 11.25 mg group and 0.26 microg/L in 3.75 mg group (P > 0.05). 13.8% and 17.7% of adverse events were recorded respectively in two groups, and no differences were found (P = 0.547).

CONCLUSIONAs a new long-acting sustained release formulation, triptorelin 11.25 mg is comparable to triptorelin 3.75 mg formulation in the aspect of efficacy and safety for the treatments of metastatic prostate cancer.

Adult ; Aged ; Aged, 80 and over ; Antineoplastic Agents, Hormonal ; administration & dosage ; therapeutic use ; Gonadotropin-Releasing Hormone ; analogs & derivatives ; therapeutic use ; Humans ; Male ; Middle Aged ; Prostatic Neoplasms ; drug therapy ; pathology ; Safety ; Treatment Outcome ; Triptorelin Pamoate ; administration & dosage ; therapeutic use