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PubMed2005

Melengestrol acetate in experimental diets as an effective alternative to induce a decline in egg production and reversible regression of the reproductive tract in laying hens. I. Determining an effective concentration of melengestrol acetate.

Induced molting increases egg quality and egg production and extends the productive life of hens. Molting is accomplished by feed withdrawal, which has been criticized for not addressing hen well-being, and current alternatives have resulted in poor postmolt performance and inadequate well-being. Molting leads to regression of follicles on the ovary and causes loss of steroidogenic support for the oviduct, leading to cessation of lay. Melengestrol acetate (MGA), an orally active progestin, may decrease support for the ovary, resulting in loss of support for the oviduct, while hens are fed a balanced diet. In this experiment, a dose response study, Hy-Line W-36 hens were fed 0, 0.1, 1, 4, or 8 mg of MGA per hen/d in a balanced diet for 28 d and then returned to a normal diet. Four birds on d 0 and 4 birds per treatment on d 1, 2, 4, 8, 12, 16, 20, 24, 28, 32, 36, 40, and 44 were euthanized. The weight of the ovary with follicles, magnum, shell gland, and oviduct were determined. A decrease in egg production was observed in those groups receiving 4 and 8 mg of MGA, until removal of MGA from the diet. After d 28, egg production increased to the production level of hens fed 0, 0.1, or 1 mg of MGA. The weight of the ovary with follicles, oviduct, magnum, and shell gland were unchanged throughout in groups fed 0, 0.1, or 1 mg of MGA. However, groups fed 4 or 8 mg of MGA exhibited a decrease (P < 0.05) in the weight of the ovary with follicles, oviduct, magnum, and shell gland until d 28. Recrudescence of the large yellow follicles as well as rejuvenation of the oviduct and its components, the magnum and shell gland, in the 4 and 8 mg MGA groups occurred by d 44. Melengestrol acetate, fed to hens on a balanced layer diet, caused reversible regression of follicles and, therefore, removal and return of support for the oviduct.

Aging↗
PubMed2005

Pure red cell aplasia in a prostate cancer patient treated with leuprolide acetate and chlormadinone acetate.

Pure red cell aplasia (PRCA) is characterized by anemia with reticulocytopenia but with normal leukocyte and platelet counts, and a bone marrow with a selective absence of erythroid precursor cells. Drug-induced PRCA is a rare secondary form of PRCA, and is usually acute and fully reversible by the withdrawal of the causative drugs. We report a rare case of PRCA in a prostate cancer patient treated with combined androgen blockade (CAB) consisted of leuprolide acetate as a luteinizing hormone-releasing hormone agonist and chlormadinone acetate as an antiandrogen. This case demonstrated that these drugs could be a cause of PRCA, and suggests that regular close monitoring for anemia is needed in prostate cancer patients treated with these drugs.

Adenocarcinoma↗
PubMed1977

A comparative study of three low dose progestogens, chlormadinone acetate, megestrol acetate and norethisterone, as oral contraceptives.

Three low dose progestogens, chlormadinone acetate (0-5 mg), megestrol acetate (0-5 mg) in oil, and norethisterone (0-35 mg), taken daily, were employed as oral contraceptives in postnatal women who desired to postpone their next pregnancy for up to a year. In a lower and middle social class population net pregnancy rates (life table) were five to six per 100 woman-years, of which about half were due to failure to take the tablets. Side effects other than menstrual disturbance were few. Norethisterone was the least likely of the three preparations to lead to discontinuation because of disturbance of menstruation. There were three ectopic gestations amongst 35 pregnancies in 4500 women-months of use. Ninety-five patients with varicose veins, 15 with a history of thrombophlebitis and 23 with a history of liver disease took progestogens without relevant untoward effects.

Adult↗
PubMed1997

Simple differential detection of Entamoeba histolytica and Entamoeba dispar in fresh stool specimens by sodium acetate-acetic acid-formalin concentration and PCR.

Amoebiasis is caused by two distinct species, a pathogenic form (Entamoeba histolytica) and a nonpathogenic form (Entamoeba dispar), which are morphologically identical. Although the distinction between these two species is of great clinical importance, the methods developed for this purpose either are very time-consuming or involve laborious procedures for isolation of the DNA. We report here a simple PCR method starting with fresh stool specimen that allows for the sensitive and reliable distinction between E. histolytica and E. dispar. After initial concentration by the sodium acetate-acetic acid-formalin (SAF) method and digestion with proteinase K, a 0.88-kb sequence of the multicopy 16S rRNA gene served as a target for PCR amplification. The method starting with unpreserved specimens proved to be very sensitive and was not influenced by the quick exposure to SAF fixative during the initial concentration step. However, storage in SAF fixative prior to testing resulted in a decreased sensitivity within 2 days. The detection limit of the method was as low as one copy of the 16S rRNA gene. No cross-reactivity was observed with other common intestinal protozoa. Mixed infections involving both E. histolytica and E. dispar could easily be detected at a ratio of 1:10,000 by agarose gel electrophoresis or a DNA hybridization immunoassay.

Acetic Acid↗
PubMed2004

Neoadjuvant hormone treatment with leuprolide acetate depot 3.75 mg and cyproterone acetate, before radical prostatectomy: a randomized study.

OBJECTIVES: To assess the effect of neoadjuvant hormone treatment before radical prostatectomy on: tumor/prostate volume, prostate-specific antigen (PSA) and testosterone levels, surgical margin status and tumor stage, and the ease of surgery following treatment. METHODS: Patients with clinically localized prostatic carcinoma were randomized to receive leuprolide acetate depot 3.75 mg once a month for 3 months and cyproterone acetate 300 mg once a week for 3 weeks prior to surgery (group A). A control group of patients had surgery without any pretreatment (group B). RESULTS: 167 patients were evaluated for the efficacy parameters. In group A, 31% of patients had a reduction in tumor/prostate volume following hormone therapy. PSA and testosterone levels were significantly reduced (p = 0.0001) in patients in group A compared to basal values. Centralized histopathological data evaluated in 145 patients (group A and 75 group B) showed that more patients in group B had tumors at stages T3A and T3B than in group A; this difference was close to significance (p = 0.057). Positive surgical margins were more common in group B (60% of patients) compared to group A (39% of patients). Similarly lymph node involvement was more common in group B compared to group A (11 versus 3%). There was little difference between the 2 study groups for the other surgical parameters assessed (ease of dissection, duration of surgery, blood loss). CONCLUSIONS: Neoadjuvant hormone therapy before radical prostatectomy has some effects in the treatment of prostate cancer. However, long-term follow-up of patients is needed to assess the impact of this therapy on morbidity and mortality.

Adenocarcinoma↗
PubMedDate not supplied

1'-Acetoxychavicol acetate, a superoxide anion generation inhibitor, potently inhibits tumor promotion by 12-O-tetradecanoylphorbol-13-acetate in ICR mouse skin.

The anti-tumor-promoting activity of 1'-acetoxychavicol acetate (ACA) was examined in a two-stage carcinogenesis experiment in ICR mouse skin using 7,12-dimethylbenz[a]anthracene (0.19 mumol) and 12-O-tetradecanoylphorbol-13-acetate (TPA; 1.6 nmol). Topical application of ACA (160 nmol) markedly reduced the average number of tumors per mouse and the ratio of tumor-bearing mice: inhibition ratios 90% (p < 0.001) and 42% (p < 0.005), respectively. ACA even at a dose equimolar to TPA (1.6 nmol) significantly reduced the average number of tumors per mouse: inhibitory ratio 44% (p < 0.05). ACA potently inhibited TPA-induced superoxide (O2-) generation in differentiated HL-60 cells (IC50 = 4.3 microM) and suppressed the lipid hydroperoxide formation by 42% (p < 0.001) in the ethyl linoleate autoxidation test.

Animals↗
PubMed1997

Differential effects of hormone-replacement therapy on endogenous nitric oxide (nitrite/nitrate) levels in postmenopausal women substituted with 17 beta-estradiol valerate and cyproterone acetate or medroxyprogesterone acetate.

Increased incidence of cardiovascular disease in postmenopausal women (PMW) is accompanied by ovarian dysfunction; hormone replacement therapy (HRT) can have cardioprotective effects. Because hypertension and atherosclerosis are associated with impaired release of endothelium-derived nitric oxide (NO) and increased levels of low-density lipoproteins (LDL), we investigated whether HRT augments NO release, and whether these increases are accompanied by a decrease in LDL levels in PMW. We determined serum nitrite/ nitrate (NO2-/NO3-) and LDL levels at baseline (before initiation of HRT) and during the 6th and 12th months of the study. The PMW (n = 26) received continuous oral administration of estradiol valerate (Progynova, 2 mg daily) for 21 days supplemented with either oral cyproterone acetate (CPA; 1 mg; n = 11) or medroxyprogesterone acetate (MPA; 5 mg; n = 15) on days 12-21 of each treatment cycle. Blood samples in the PMW receiving HRT were collected at times while the subjects were taking estradiol valerate alone and estradiol valerate plus CPA or MPA. Compared with the samples collected at baseline, serum NO2-/NO3- levels increased significantly from 20.1 +/- 1.58 mumol/L at baseline to 30 +/- 3.7 mumol/L (P < 0.01) in samples collected after 12 months of HRT while the PMW were not taking progestins (CPA or MPA), and to 25.4 +/- 2 mumol/L (P < 0.05) when all the samples, regardless of the treatment with CPA or MPA, were included in the analysis. Moreover, > 30% increase in serum NO2-/NO3- levels were observed only in 13 (responders) out of 26 PMW substituted with estradiol valerate, suggesting that estradiol may improve endogenous NO synthesis in a differential fashion. Compared with baseline, no significant increases in serum NO2-/NO3- were observed in samples collected while the estradiol-treated responders were taking either CPA or MPA. In contrast to NO2-/NO3- serum LDL levels were significantly reduced in samples collected after 12 months of HRT (P < 0.05 vs. baseline). Furthermore, levels of NO2-/NO3 showed a significant negative correlation with the levels of LDL (r2 = 0.17; P < 0.05) in the responders but not in nonresponders. These results indicate that oral administration of estradiol valerate in PMW for HRT increases circulating NO levels, an effect that may contribute to the cardioprotective effects of HRT in PMW. In addition, our data suggests but does not prove that concomitant administration of a progestin may attenuate the beneficial effects of estrogen replacement therapy with regard to NO release. Finally, our data provides evidence for the existence of responders and nonresponders to postmenopausal estrogen treatment with respect to improvement of endogenous NO levels, suggesting that a significant number, but not all, of the hormonally substituted PMW profit fully from the beneficial properties of a HRT.

Estradiol↗
PubMed1991

Aryloxy acetic acid diuretics with uricosuric activity. I. Polycyclic aryloxy acetic acids.

In order to obtain lead compounds for uricosuric diuretics, various polycyclic aryloxy acetic acids [isoindole derivative (7), quinazoline derivative (15), benzopyran derivative (20), xanthone derivative (24), benzofuran derivative (30) and indene derivative (36)] were prepared. These compounds were evaluated for diuretic activity in rats, uricosuric activity in rats and antihypertensive activity in 11-deoxycorticosterone acetate (DOCA)/salt hypertensive rats. Among the compounds, 20 showed potent diuretic, uricosuric and moderate antihypertensive activities. Therefore, we selected 20 as a lead compound for development of new uricosuric diuretics.

Acetates↗
PubMed2006

Synthesis and anti-tumor activity of a fluorinated analog of medroxyprogesterone acetate (MPA), 9alpha-fluoromedroxyprogesterone acetate (FMPA).

We synthesized 9alpha-fluoromedroxyprogesterone acetate (FMPA) in order to test whether it is a more potent anti-angiogenic agent than medroxyprogesterone acetate (MPA), which has been widely used as a therapeutic agent for breast and endometrium cancers. FMPA was previously synthesized in 10 steps (total yield: 1%). An efficient synthesis of FMPA has been achieved in 6 steps (total yield: 12%). We examined the anti-tumor effect of FMPA, complexed with dimethyl-beta-cyclodextrin (DM-beta-CyD), on rat mammary carcinomas induced by 7,12-dimethylbenz[a]anthracene (DMBA). FMPA showed great anti-tumor effect on DMBA-induced rat mammary carcinomas.

Administration, Oral↗
PubMed1988

A reversed-phase high-performance liquid chromatographic method for the simultaneous determination of serum concentrations of cyproterone acetate and 15 beta-hydroxycyproterone acetate.

A reversed-phase high-performance liquid chromatographic method for the simultaneous determination of cyproterone acetate (CPA), 15 beta-hydroxycyproterone acetate (15 beta-OH-CPA) and cyproterone (CP) was reported. This method was specific, sensitive, precise, easy and rapid for determination of the serum concentrations of these steroids in patients receiving CPA. Although no peak corresponding to CP was observed for serum, peaks corresponding to CPA and 15 beta-OH-CPA were detected and well separated in all subjects undergoing long-term CPA therapy. In these patients, there seemed to be a dose-dependent relationship between the amount of CPA administered and the serum concentrations of these steroids, and the serum concentrations of CPA were either similar or low compared with those of 15 beta-OH-CPA. In conclusion, this simplified method is thought to be very valuable for studies on the pharmacokinetics of CPA and 15 beta-OH-CPA, and on the relationship between the CPA dosage and the therapeutic or side effects on adrenal and gonadal steroid production.

Administration, Oral↗
PubMed2000

Inhibition of disease flare with diethylstilbestrol diphosphate and chlormadinone acetate administration for two weeks prior to slow-releasing leuprolide acetate in prostatic cancer patients.

To determine whether administration of estrogen or gestagen prior to luteinizing hormone-releasing hormone (LH-RH) agonist prevents disease flare in prostate cancer patients, we pretreated the patients with either diethylstilbestrol diphosphate (DES-P) 300 mg daily (N = 17) or chlormadinone acetate (CMA) 100 mg daily (N = 16) or none (N = 16) for two weeks before the initial injection of leuprolide acetate (L). Blood samples for prostatic specific antigen (PSA), testosterone (T), and luteinizing hormone were collected before CMA and DES-P administration, before and at 2, 7, 14, 28, 56, and 84 days after the first administration of leuprolide. The treatment with DES-P and CMA prior to LH-RH agonist induced an early decline of PSA. The mean PSA level showed no significant secondary rise in those patients with pretreatment after L administration. In the patients pretreated with DES-P or CMA, the mean serum T level never exceeded the pretreatment baseline after L administration. On the other hand, in the patients without DES-P or CMA, both serum T and PSA levels increased after the first administration of L. These results clearly demonstrate that pretreatment with DES-P 300 mg daily or CMA 100 mg daily for 2 weeks is quite effective to prevent disease flare after the first administration of L in patients with prostatic cancer.

Aged↗
PubMed2001

European/Canadian multicenter, double-blind, randomized, placebo-controlled study of the effects of glatiramer acetate on magnetic resonance imaging--measured disease activity and burden in patients with relapsing multiple sclerosis. European/Canadian Glatiramer Acetate Study Group.

Two prior double-blind, placebo-controlled, randomized trials demonstrated that glatiramer acetate (GA) reduces relapse rates in patients with relapsing remitting multiple sclerosis (RRMS). This study was designed to determine the effect, onset, and durability of any effect of GA on disease activity monitored with magnetic resonance imaging (MRI) in patients with RRMS. Two hundred thirty-nine eligible patients were randomized to receive either 20 mg GA (n = 119) or placebo (n = 120) by daily subcutaneous injection. Eligibility required one or more relapses in the 2 years before entry and at least one enhancing lesion on a screening MRI. The study was a randomized, double-blind, placebo-controlled phase during which all patients studied underwent monthly MRI scans and clinical assessments over 9 months. The primary outcome measure was the total number of enhancing lesions on T1-weighted images. Secondary outcome measures included the proportion of patients with enhancing lesions, the number of new enhancing lesions and change in their volume; the number of new lesions detected on T2-weighted images and change in their volume, and the change in volume of hypointense lesions seen on unenhanced T1-weighted images. Clinical measures of disease activity were also evaluated. The active treatment and placebo groups were comparable at entry for all demographic, clinical, and MRI variables. Treatment with GA showed a significant reduction in the total number of enhancing lesions compared with placebo (-10.8, 95% confidence interval -18.0 to -3.7; p = 0.003). Consistent differences favoring treatment with GA were seen for almost all secondary end points examined: number of new enhancing lesions (p < 0.003), monthly change in the volume of enhancing lesions (p = 0.01), and change in volume (p = 0.006) and number of new lesions seen on T2-weighted images (p < 0.003). The relapse rate was also significantly reduced by 33% for GA-treated patients (p = 0.012). All effects increased over time. Glatiramer acetate significantly reduced MRI-measured disease activity and burden.

Adult↗
PubMed1975

The identification of phorbolol myristate acetate as a new metabolite of phorbol myristate acetate in mouse skin.

Aspects of the metabolism of phorbol myristate acetate (PMA) in mouse skin were investigated. Phorbolol myristate acetate (PHMA), a potential metabolite of PMA in mouse skin, was prepared from PMA by NaBH4 reduction of the C-5 carbonyl group of PMA to a secondary alcohol. The structure of PHMA was assigned on the basis of spectral and chemical evidence. PHMA had an inflammatory effect in mouse skin equal to or slightly less than PMA, on the basis of the dermal infiltration of lymphocytes and neutrophils and interfollicular epidermal hyperplasia. Application of PHMA and PMA to mouse skin resulted in equal increases in numbers of interfollicular epidermal basal layer mitotic cells after 28 hr. PHMA was found to be nearly as effective as PMA in increasing the incorporation of [3H]thymidine into interfollicular epidermal basal layer cells after 28 hr. When tritiated PMA was applied to mouse skin, PHMA was identified as a metabolite. PHMA was present in about 1.7% of the amount of PMA. When tritiated PHMA was applied to mouse skin, PMA was not detected as a metabolite in the mouse skin extracts.

Animals↗
PubMed1992

Antiproliferative effect of leuprorelin acetate, alone or combined with tamoxifen or medroxyprogesterone acetate, on human breast cancer cell lines.

We have investigated the antiproliferative action of leuprorelin acetate (TAP-144) on human breast cancer cells, cultured in medium supplemented with charcoal-treated fetal calf serum. The analogue had no effect on cell growth of oestrogen receptor-negative MDA-MB-231 cells. Although ineffective when used alone, TAP-144 inhibited in a dose-dependent fashion the oestradiol-induced cell growth in oestrogen receptor-positive and oestrogen-sensitive MCF-7, ZR-75-1 and CG-5 cells. TAP-144 did not modify the growth inhibitory activity of tamoxifen on CG-5 cells. A high concentration of TAP-144 (10(-6) M) seemed to increase the antioestrogenic effect of medroxyprogesterone acetate (MPA) (10(-7) M) in the same model. The data reported indicate that, in our culture conditions, TAP-144 has a direct antitumour effect on breast tumour cells. Our findings concerning the promotion of the antiproliferative effect of MPA merit further investigation.

Antineoplastic Agents↗
PubMed1991

[Determination of megestrol acetate and estradiol valerate in injection of microencapsulated compound megestrol acetate by secondary derivative spectrophotometry].

The paper reports the simultaneous determination of megestrol acetate and estradiol valerate in the injection of microencapsulated compound megestrol acetate by secondary derivative spectrophotometry. The experimental results showed that the average recoveries of the two drugs were 98.8% and 98.0%, respectively, and that the coefficients of variation were 0.71% and 1.81%, respectively.

Capsules↗
PubMed1988

Pharmacokinetics of cyproterone acetate and its main metabolite 15 beta-hydroxy-cyproterone acetate in young healthy women.

Cyproterone acetate (CPA) and 15 beta-hydroxy-cyproterone acetate (15 beta-OH-CPA) have been quantitated in human plasma by a selective, automated HPLC assay in 8 young female subjects. Subjects received a single oral dose of 100 mg CPA and four weeks later, a single intramuscular dose of 300 mg CPA. Plasma levels in seven subjects could be evaluated pharmacokinetically. After intramuscular administration maximum CPA serum levels of 191 +/- 49 ng/ml were reached between 2 and 3 days. Postmaximal levels declined with a half-life of 4.3 +/- 0.7 days. After oral administration maximal serum levels of 255 +/- 110 ng/ml were measured between 2 and 3 h. CPA levels decayed biphasically with a terminal half-life of 3.6 +/- 1.3 days. Bioavailability after oral administration was nearly complete (88 +/- 20%). Metabolite levels were below CPA levels until 4 days (i.m.) and 6 h (p.o.) and exceeded CPA levels later on. 15 beta-OH-CPA levels declined with half-lives similar to those of corresponding CPA levels, indicating that terminal half-life of the metabolite in serum reflects its rate of formation rather than its rate of elimination. Areas under the metabolite serum level curves after intramuscular and oral administration were 10 to 15% higher than the corresponding areas for unchanged CPA. Since CPA and 15 beta-OH-CPA contribute to the antiandrogenetic efficacy there is good reason to assume that the intramuscular administration of CPA might be equally effective in the therapeutical use as the oral administration.

Administration, Oral↗