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PubMed2002

Antifungal activity of sodium acetate and Lactobacillus rhamnosus.

The inhibition of molds by sodium acetate in deMan Rogosa Sharpe (MRS) medium, along with the antifungal activity of Lactobacillus rhamnosus VT1, was studied by the slope agar plate method. MRS agar prepared with and without sodium acetate was used as the agar substrate. A total of 42 strains of Aspergillus, Penicillium, Fusarium, Alternaria, Cladosporium, and Rhizopus were used to compare sensitivities to the inhibitory activity of sodium acetate and L. rhamnosus VT1. It was found that sodium acetate in MRS medium affected the growth of 33 of the 42 mold strains tested to various degrees. The highest sensitivity to sodium acetate was shown by strains of Fusarium, followed by strains of Penicillium, Aspergillus, and Rhizopus. L. rhamnosus VT1 also inhibited mold growth. A significant finding was that sodium acetate and L. rhamnosus VT1 in combination exhibited a possible synergistic action. Thirty-nine of the 42 mold strains tested were completely inhibited by the presence of both antifungal agents. This finding confirms that sodium acetate, a basic component of commercial MRS medium, has strong antifungal properties, and this must be taken into consideration when evaluating the antifungal activity of Lactobacillus cultures grown in MRS broth.

Agar↗
PubMed1999

Inhibition of mucosal glycylsarcosine uptake by acetate in rat distal small intestine.

Acetate deriving from microbial fermentation may occur at considerable concentrations in the distal small intestine, where it appears to be absorbed by two different mechanisms: acetate-HCO3- exchange and non-ionic diffusion. Whether acetate affects absorption of other nutrients at this intestinal site is not known. Therefore the influence of acetate (30 mmol l-1) on oligopeptide absorption was studied using an in vitro mucosal uptake technique allowing measurement of substrate uptake across the brush border membrane (BBM). Acetate significantly inhibited mucosal uptake of 14C-labelled glycylsarcosine (Gly-Sar) at pH 6 and pH 7 in the presence of sodium. No inhibition occurred in the absence of sodium. Both acetate and the absence of sodium decreased Vmax of mucosal Gly-Sar uptake without substantially affecting the apparent Km value. Since it is well established that Vmax of peptide transport across the intestinal BBM depends on the size of the transmembrane H+ gradient as a driving force the present findings are in accordance with the assumption that acetate inhibits peptide absorption by attenuating the H+ gradient across the BBM, which depends on the presence of sodium.

Acetic Acid↗
PubMedDate not supplied

[Dark metabolism of acetate in Rhodospirillum rubrum cells, grown under photoheterotropic conditions].

The mechanism of the dark assimilation of acetate in the photoheterotrophically grown nonsulfur bacterium Rhodospirillum rubrum was studied. Both in the light and in the dark, acetate assimilation in Rsp. rubrum cells, which lack the glyoxylate pathway, was accompanied by the excretion of glyoxylate into the growth medium. The assimilation of propionate was accompanied by the excretion of pyruvate. Acetate assimilation was found to be stimulated by bicarbonate, pyruvate, the C4-dicarboxylic acids of the Krebs cycle, and glyoxylate, but not by propionate. These data implied that the citramalate (CM) cycle in Rsp. rubrum cells grown aerobically in the dark can function as an anaplerotic pathway. This supposition was confirmed by respiration measurements. The respiration of cells oxidizing acetate depended on the presence of CO2 in the medium. The fact that the intermediates of the CM cycle (citramalate and mesaconate) markedly inhibited acetate assimilation but had almost no effect on cell respiration indicative that citramalate and mesaconate are intermediates of the acetate assimilation pathway. The inhibition of acetate assimilation and cell respiration by itaconate was due to its inhibitory effect on propionyl-CoA carboxylase, an enzyme of the CM cycle. The addition of 5 mM itaconate to extracts of Rsp. rubrum cells inhibited the activity of this enzyme by 85%. The data obtained suggest that the CM cycle continues to function in Rsp. rubrum cells that have been grown anaerobically in the light and then transferred to the dark and incubated aerobically.

Acetates↗
PubMed2003

Acetate metabolism in brain mechanisms of adaptation to ethanol.

BACKGROUND: The aim of this study was to estimate the role of acetate-induced metabolic changes in brain mechanisms of resistance to the narcotic effect of ethanol. MATERIAL/METHODS: Wistar rats were treated daily with ethanol (3.5 g/kg i.p. for 7 days). During alcohol treatment, the duration of ethanol-induced sleep was decreased. Levels of acetate, acetyl-CoA, adenosine, and the pool of AMP+ADP, and the activity of acetyl-CoA synthetase and 5'-nucleotidase in the brain were measured. Synaptosomal adenosine and acetylcholine release were measured in the presence of acetate, adenosine and 2-chloroadenosine. RESULTS: The concentration of acetate was higher in all investigated brain regions of ethanol rats in comparison to controls. The activity of acetyl-CoA synthetase and 5'-nucleotidase, as well as the levels of adenosine and the pool of AMP+ADP were raised in cerebral cortex of ethanol rats. The synaptosomal level of adenosine was higher in control rats. Acetate caused a 3-fold increase of extrasynaptosomal adenosine level. Synaptosomes from ethanol rats showed higher rates of Ca-dependent releases of acetylcholine. 2-chloradenosine resulted in inhibition of synaptic acetylcholine release only in control rats. CONCLUSIONS: Ethanol causes an increase of acetate in brain and adenosine level in cerebral cortex. Acetate causes an increase of the extrasynaptic adenosine level. Prolonged ethanol treatment results in an increase of synaptic Ca-dependent acetylcholine release. Seven-day treatment with ethanol eliminates the inhibitory effect of 2-chloroadenosine-A1 adenosine receptor agonist on synaptic Ca-dependent acetylcholine release.

Acetic Acid↗
PubMedDate not supplied

Acetate free biofiltration. Effects on peripheral blood monocyte activation and cytokine release.

Acetate free biofiltration (AFB), a new hemodiafiltration (HDF) technique characterized by a buffer free dialysate and postdilution infusion of a sterile HCO3 solution, was recently proposed as an alternative to HDF performed with acetate or bicarbonate dialysate. To evaluate the effects of dialysate buffer on immune cell activation, release of interleukin-1 (IL-1), tumor necrosis factor (TNF), prostaglandin E2 (PGE2), and leukotriene B4 (LTB4) from peripheral blood monocytes was studied in 12 uremic patients before and after HDF with polyacrylonitrile membranes (Filtral 12, Hospal Laboratories, Bologna, Italy) and consecutive dialysis with acetate, bicarbonate, and AFB. Data were correlated with the monocyte cytoplasmic concentration of Ca++, an index of early cell activation. Levels of bacterial endotoxins in the acetate, bicarbonate, buffer free dialysate, and infusate for AFB were also determined. Results showed that release of IL-1, PGE2, and LTB4, was greater after HDF with acetate than with bicarbonate; after bicarbonate dialysis, however, TNF production was significantly higher. On the other hand, after AFB, minimal production of these cytokines was seen and TNF, in particular, was undetectable. There was a direct correlation between release of cytokines in the monocytes and cytoplasmic Ca++ content. In the bicarbonate dialysate, detectable levels of bacterial endotoxins were found, whereas the acetate, buffer free dialysate, and infusate were endotoxin free. It was concluded that acetate dialysis directly activates peripheral blood monocytes to produce IL-1, PGE2, and LTB4, whereas bicarbonate induced TNF activation occurs through endotoxins. In AFB, which uses a buffer free dialysate and sterile bicarbonate infusion, monocyte activation is negligible.

Acetates↗
PubMed2004

Radiation dose estimates in humans for (11)C-acetate whole-body PET.

UNLABELLED: 11C-Acetate is currently being investigated as a new tracer for imaging neoplasms, most notably prostate cancer and its metastases. Previously reported dose estimates for (11)C-acetate prepared by the Oak Ridge Institute for Science and Education (ORISE) were based on a simple 3-compartment model in which all activity not measured in blood or excretion via breath was assumed to reside in the heart. Because all organs are involved in acetate metabolism to some extent, these estimates might overestimate heart and underestimate other organ dosimetry. Dynamic whole-body (11)C-acetate PET was therefore performed on 6 healthy human volunteers. Measured dose estimates for all target organs were compared with the existing ORISE values. METHODS: After transmission scanning had been performed for measured attenuation, 525 MBq of (11)C-acetate were injected intravenously, and 5 sequential whole-body emission scans were obtained from the head to mid thighs. Regions of interest were drawn to encompass the entire activity in all visible organs at each time point. Time-activity data were fit in a least-squares sense to obtain residence times. Absorbed dose estimates were determined using MIRDOSE3.1 software. RESULTS: The effective dose was 0.0049 mSv/MBq. The organs receiving the highest absorbed doses were the pancreas (0.017 mGy/MBq), bowel (0.011 mGy/MBq), kidneys (0.0092 mGy/MBq), and spleen (0.0092 mGy/MBq). No urinary excretion of tracer was measurable. CONCLUSION: Using these new estimates for (11)C-acetate dosimetry, the maximum injected activity under Radioactive Drug Research Committee limits can be raised up to 5-fold over the limit imposed by the previous ORISE estimates. A higher injected activity would improve counting statistics and, it is hoped, overall image quality and tumor detection with whole-body (11)C-acetate PET.

Acetates↗
PubMedDate not supplied

Correlation between intradialytic hypotension in patients undergoing routine hemodialysis and use of acetate compared in bicarbonate dialysate.

AIM: To determine the incidence of intradialytic hypertension (IDH) during hemodialysis (HD) in end-stage renal disease (ESRD) patients using acetate dialysate compared to those using bicarbonate dialysate. METHODS: This study was a double-blind cross-over randomized clinical trial. The effect of acetate and bicarbonate dialysate on blood pressure was analyzed in two consecutive HD sessions. The selected subjects were 41 stable ESRD patients scheduled for dialysis 2 times/week/from the HD unit of Dr.Soetom Hospital Surabaya, aged between 21-65 years old, with a hemoglobin level > or = 7 g/dL, serum albumin > or = 3 mg/dL and interdialytic weight gain < 4 Kg, and an average Qb 150-250 ml/minute. The dialysate sodium level was 138 mEq/L/ The study subjects were divided into tow groups: 21 patients in the group who received Acetate on the first session and Bicarbonate on the next (AB) and 20 patients in the group receiving Bicarbonate first (BA). Comparison of IDH during use of each dialysate was analyzed by Chi-Square and Mc Nemar Chi-Square test. RESULTS: No characteristic differences were found in both groups: HD duration (for AB) was 28.83 +/- 13.89 vs. 34.95 +/- 24.80 months (for BA) (p = 0.333); Age (for AB) was 47.61 +/- 9.49 vs. 47.75 +/- 11.80 years (for BA) (p = 0.969); Hemoglobin (Hb) level (for AB) 8.19 +/- 0.84 vs. 7.94 +/- 0.41 mg/dL (for BA) (p = 0.238); serum Albumin (for AB) was 3.79 +/- 0.26 vs. 3.82 +/- 0.30 g/dl (for BA) (p = 0.652). The number of patients with IDH during acetate dialysate with IDH during bicarbonate dialysate was 1 (2.4%). Overall, there were 11 patients with Diabetic Kidney Disease (26.8%). Six out of them (54.5%) had IDH during acetate dialysate and only and 1 patient (9.1%) had IDH during acetate and bicarbonate. CONCLUSION: The incidence of IDH in hemodialysis using acetate is significantly greater than that when bicarbonate is used (p = 0.000).

Acetates↗
PubMed2006

Butyrate production from oligofructose fermentation by the human faecal flora: what is the contribution of extracellular acetate and lactate?

Butyrate is an important substrate for maintenance of colonic health and oligofructose fermentation by human faecal bacteria can increase butyrate production in vitro. However, oligofructose appears to be fermented by mainly acetate and lactate-producing bacteria rather than butyrate-producing bacteria. Isotope labelling studies using [U-(13)C(6)]glucose were used to show that (13)C(2) and (13)C(4) were the major labelled butyrate species produced from glucose fermentation, via [(13)C(2)]acetate-acetyl CoA as intermediate. Bacterial interconversion reactions were quantified and acetate conversion to butyrate and lactate conversion to acetate, propionate and butyrate were observed. Addition of oligofructose to faecal batch cultures significantly increased butyrate production. Of the newly synthesised butyrate from oligofructose fermentation, 80 % was derived from interconversion of extracellular acetate and lactate, with acetate being quantitatively more significant. Carbohydrates, such as oligofructose, have prebiotic properties. In addition, oligofructose selectively stimulates the bacterial conversion of acetate and lactate to butyrate. Carbohydrates with similar properties represent a refinement of the prebiotic definition, termed butyrogenic prebiotics, because of their additional functionality.

Acetates↗
PubMed1990

Cerebral metabolism of [1,2-13C2]acetate as detected by in vivo and in vitro 13C NMR.

The metabolism of [1,2-13C2]acetate in rat brain was studied by in vivo and in vitro 13C NMR spectroscopy, in particular by taking advantage of the homonuclear 13C-13C spin coupling patterns. Well nourished rats were infused with [1,2-13C2]acetate or [1-13C]acetate in the jugular vein, and the in situ kinetics of 13C labeling during the infusion period was followed by 13C NMR techniques. The in vivo 13C NMR spectra showed signals from (i) the C-1 carbon of [1,2-13C2] acetate or [1-13C]acetate, (ii) 13CO3H-, and (iii) the natural abundance 13C carbons of sufficiently mobile fatty acids. Methanol/HCl/perchloric acid extracts of the brains were prepared and were further analyzed by high resolution 13C NMR. The homonuclear 13C-13C spin coupling patterns after infusion of [1,2-13C2]acetate showed very different isotopomer populations in glutamate, glutamine, and gamma-aminobutyric acid. Analyzing the relative proportions of these isotopomers revealed (i) two different glutamate compartments in the rat brain characterized by the presence and absence, respectively, of glutamine synthase activity, (ii) two different tricarboxylic acid cycles, one preferentially metabolizing [(1,2-13C2]acetate, the other mainly using unlabeled acetyl-coenzyme A, (iii) a hitherto unknown cerebral pyruvate recycling system associated with the tricarboxylic acid cycle, metabolizing primarily unlabeled acetyl-coenzyme A, and (iv) a predominant production of gamma-aminobutyric acid in the glutamate compartment lacking glutamine synthase.

Acetates↗
PubMed1990

Net ultrafiltration volume (nUFV) during IPD with acetate or lactate dialysis solutions.

There is debate as to how much acetate in PD solutions influences the nUFV, so we decided to evaluate it during uncomplicated IPD and aseptic peritonitis connected with IPD treatment. In 8 patients dialysed with acetate (35 mmol/L) solutions for 9 +/- 8 months the nUFV (drainage volume minus instillation volume, mL/exchange) was calculated for 1.5 and 4.25% glucose exchanges during uncomplicated IPD and aseptic peritonitis. Then, lactate (35 mmol/L) buffered solutions were used instead of acetate ones and the nUFV was estimated under the same conditions. During uncomplicated IPD as well as peritonitis the nUFV was significantly higher in exchanges with lactate then with acetate solutions when the glucose concentration were comparable. In aseptic peritonitis the nUFV was less decreased with lactate than acetate solutions. We conclude during uncomplicated IPD or aseptic peritonitis in patients dialysed with acetate buffer the nUFV can be improved when acetate in PD solutions is substituted by lactate.

Acetates↗
PubMed1989

Effect of acetate infusion on energy expenditure and substrate oxidation rates in non-diabetic and diabetic subjects.

Sodium acetate was infused intravenously at 2.5 mmoles/min for 60 min into 6 normal subjects and 6 non-insulin dependent diabetic patients. In control experiments the same subjects received equimolar sodium bicarbonate infusions. Plasma non-esterified fatty acid and blood glycerol levels fell during acetate infusion in both groups, suggesting impairment of lipolysis. The respiratory quotient fell on acetate infusion as expected, although total energy expenditure was unaffected. If acetate oxidation was assumed to be 90 per cent of the infusion rate, then it accounted for about 40 per cent of total oxygen consumption; fat oxidation was reduced, whilst carbohydrate oxidation was unchanged. These results suggest that resting energy expenditure is maintained during acetate infusion since acetate replaces fat as an oxidative fuel, without affecting glucose oxidation. The reduction in fat oxidation appears to be due to reduced fat mobilization from adipose tissue. The metabolic effects of acetate infusion are similar in normal and in non-insulin dependent diabetic subjects.

Acetates↗
PubMed1978

Inhibition of DNA synthesis by 1,2-dimethylhydrazine and methylazoxymethanol acetate in rabbit colon mucosa in organ culture.

When maintained in organ culture, colon mucosa from male New Zealand White rabbits showed a near-normal mucosal morphology and linear incorporation of [3H]thymidine into mucosal DNA up to 36 hours of incubation. Explants from the descending colon had a higher DNA synthetic activity than did other segments of the large bowel. Inhibition of DNA synthesis in colon explants by 1,2-dimethylhydrazine (DMH) and methylazoxymethanol (MAM) acetate was dose-dependent. When DNA synthesis was determined after an 18-hour incubation, MAM acetate inhibited DNA synthesis at concentrations of 50, 100, 150, and 200 microgram/ml. With the same concentration of DMH, little or no inhibition was observed. At the concentration of 200 microgram/ml, both carcinogens significantly inhibited DNA synthesis after 3 and 6 hours of incubation. With longer incubation, the inhibitory effect of DMH appeared to be reversible, whereas DNA synthesis was continuously inhibited by MAM acetate up to 18 hours of incubation. No altered uptake of [3H]thymidine by colon explants incubated in the presence of DMH or MAM acetate for 18 hours was observed. No morphologic changes were seen in colon explants treated with 200 microgram MAM acetate/ml for 18 hours. Physostigmine sulfate had no influence on MAM acetate-induced inhibition of DNA synthesis in colon explants. These in vitro observations reflected a direct action of DMH and MAM acetate on the colon mucosa and supported the possibilility that colon epithelial cells contain enzymes capable of activating DMH and MAM acetate to their alkylating carcinogens.

Animals↗
PubMed1985

Comparison of the actions of RU 38486 and megestrol acetate in the model of a transplantable adrenocorticotropin- and prolactin-secreting rat pituitary tumor.

The effects of the progesterone antagonist RU 38486 and the progesterone agonist megestrol acetate on the growth of the estrogen-progesterone receptor-positive transplantable adrenocorticotropin (ACTH)/prolactin-secreting rat pituitary tumor 7315a were examined. RU 38486 (2.5 mg/kg/day) for 30 days significantly inhibited tumor size, tumor weight, and the plasma prolactin and ACTH concentrations, while the same dose of megestrol acetate only inhibited pituitary tumor weight. Megestrol acetate inhibited both the release and total ACTH content of the anterior pituitary gland, while RU 38486 increased both the release and the total ACTH content. Studies with ACTH secretion by cultured normal rat pituitary cells showed that megestrol acetate (1 microM) did not affect corticotropin-releasing factor (CRF)-stimulated ACTH release after 4-hr exposure, but inhibited CRF-stimulated ACTH release by 50% after 24-hr preincubation. The glucocorticoid-like effect of 1 microM megestrol acetate in this model is similar to that exerted by 10 nM dexamethasone. Acute exposure or preincubation of rat pituitary cells with RU 38486 (1 microM) did not influence CRF-stimulated ACTH release, while preincubation for 24 hr revealed a dose-dependent reversing effect of RU 38486 on dexamethasone-induced inhibition of CRF-stimulated ACTH release. In this model, 1 microM RU 38486 completely overcame the effect of 10 nM dexamethasone. Megestrol acetate and RU 38486 have inhibitory effects on the growth of the 7315a tumor. They differ both with regard to their effects on the progesterone and the glucocorticoid receptor, with megestrol acetate exerting an agonistic and RU 38486 an antagonistic action.

Adenocarcinoma↗
PubMed1987

Suppression of cortisol responses to exogenous adrenocorticotrophic hormone, and the occurrence of side effects attributable to glucocorticoid excess, in cats during therapy with megestrol acetate and prednisolone.

The major purpose of this investigation was to determine the effect of prednisolone and megestrol acetate in cats on the adrenal cortisol response to exogenous adrenocorticotrophic hormone during drug administration at dose rates employed for management of some inflammatory feline dermatoses. Prednisolone (at least 2 mg/kg/day) and megestrol acetate (5 mg/cat/day) were each administered orally to seven cats from days 1 to 16. Three additional cats received no therapy. Basal and stimulated cortisol concentrations, food and water intake, hematology, blood biochemistry, urinalyses, and hepatic and cutaneous histology were studied in all cats before, during, and two weeks following the end of treatment. Cats given prednisolone or megestrol acetate had significant suppression of stimulated cortisol levels on day 8. This change was more marked on day 15, when the suppression in cats given megestrol acetate was also significantly more severe than in those receiving prednisolone. Recovery of adrenal reserve was considered present on day 30 in six of seven cats given prednisolone, but in only three of seven receiving megestrol acetate. Eosinopenia, glycosuria and hepatocyte swelling from glycogen deposition were occasionally recorded in treated cats of both groups, providing additional circumstantial evidence for glucocorticoid activity of megestrol acetate in cats. It is advised that abrupt withdrawal of prednisolone or megestrol acetate therapy be avoided in this species to reduce the chance of precipitating clinical signs of hypoadrenocorticism, even after treatment for as little as one week.

Adrenal Cortex↗
PubMed1986

Effects of acetate and bicarbonate dialysis on cardiac performance, transmural myocardial perfusion and acid-base balance.

The effects of acetate and bicarbonate dialysis on cardiac performance, myocardial oxygen balance and acid-base balance were evaluated in 7 patients with end-stage renal failure. During acetate dialysis cardiac output increased and was significantly higher than during bicarbonate dialysis (p less than 0.05). Systemic vascular resistance was significantly lower during acetate than during bicarbonate dialysis (p less than 0.05). The myocardial oxygen balance estimated from the supply/demand ratio (DPTI/SPTI) was significantly reduced after acetate dialysis and significantly lower than during bicarbonate dialysis (p less than 0.05). After 90 min acetate dialysis DPTI/SPTI dropped to its lowest value as a result of an excess of myocardial oxygen demand (SPTI) over myocardial oxygen supply (DPTI), signifying transient hypoperfusion of the subendocardium which did not occur during bicarbonate dialysis. Acidosis was more adequately corrected with bicarbonate dialysis, and there was no change in pCO2 which was significantly higher than during acetate dialysis (p less than 0.05). During bicarbonate dialysis a stable hemodynamic circulation and well balanced acid-base values were seen. Acetate dialysis leads to improvement in left ventricular performance, but at the expense of myocardial oxygen balance, which falls to marginal safety levels in uremic patients.

Acetates↗
PubMed1987

Cardiovascular and acid-base effects of acetate and bicarbonate haemodialysis.

Cardiovascular and acid-base changes were studied in 18 adult haemodialysis patients during a single dialysis against acetate or bicarbonate dialysate. Tachycardia was significantly greater with acetate but, otherwise, blood pressure and peripheral resistance fell and cardiac output increased to a similar degree with the two types of dialysate. Arterial PCO2 increased with bicarbonate and fell slightly with acetate, while hypoxaemia was significantly worse during acetate dialysis. Arterial acetate concentrations increased in 2 of 12 patients during bicarbonate dialysis. No differences in patient symptomatology or hypotensive episodes were noted with acetate or bicarbonate. Any beneficial effects of bicarbonate dialysis are more likely to be related to preservation of arterial PO2 than to the absence of adverse cardiovascular effects of acetate.

Acetates↗
PubMed1988

Excessive ATP degradation during hemodialysis against sodium acetate.

As the initial step in examining the metabolic basis for acetate intolerance, we have tested the hypothesis that excessive adenosine triphosphate (ATP) degradation occurs during hemodialysis against acetate dialysate (compared with the degree of degradation occurring during dialysis against bicarbonate dialysate). Seven patients undergoing long-term dialysis were infused with carbon 14--labeled 8-adenine, and their response to dialysis against acetate was compared with their response to dialysis against bicarbonate. The following changes were observed. During dialysis against acetate, the mean dialysate uric acid--to-creatinine ratio levels were significantly higher than the mean levels observed after dialysis against bicarbonate (p less than 0.001). The mean dialysate uric acid radioactivity--to-creatinine ratio and inosine, hypoxanthine, and xanthine radioactivity--to-creatinine ratio levels were significantly increased during dialysis against acetate (p less than 0.001). There was no significant change in plasma venous hypoxanthine level, but during dialysis against acetate, the arterial hypoxanthine levels (3.7 +/- 1.6 mumol/L) at 60 minutes were significantly higher than the levels observed after dialysis against bicarbonate (1.4 +/- 0.5 mumol/L) (p less than 0.01). These data provide evidence that excessive ATP degradation occurs during hemodialysis against acetate but not during hemodialysis against bicarbonate dialysate.

Acetates↗
PubMed1986

Megestrol acetate: first-line therapy for advanced breast cancer.

Megestrol acetate as initial hormonal therapy produced a 40% objective response rate in 53 patients with advanced breast cancer; another 26% achieved stable disease. For 19 patients with visceral-dominant disease, the response rate was 42%. To investigate the effect of the order of sequential hormonal therapy, records of 66 patients treated with tamoxifen before megestrol acetate or with megestrol acetate before tamoxifen were reviewed retrospectively. Of the 24 patients who were given megestrol acetate first, nine (38%) had objective response to primary therapy, and four (17%) to secondary therapy. Among the 42 patients treated with tamoxifen first, there were nine (21%) objective responses to primary therapy and eight (19%) responses to secondary therapy. Results show that megestrol acetate is effective first-line hormonal therapy for advanced breast cancer. Megestrol acetate can be used as primary hormonal therapy and tamoxifen as secondary hormonal therapy, as an alternative to the more usual reverse order. One may also consider megestrol acetate for some advanced breast cancer patients with visceral-dominant disease.

Antineoplastic Agents↗