Drugs online research references
Minerva Ginecol. 2004 Feb;56(1):15-26.
The treatment of polycystic ovary syndrome.
Ajossa S, Guerriero S, Paoletti AM, Orru M, Melis GB.
Section of Gynecology and Obstetrics and of Human Reproduction Fisiology, Department of Maternal-Infantile Surgery and Imaging Sciences, University of Cagliari, Cagliari, Italy.
Polycystic ovary syndrome (PCOS) is one of the most common endocrine disorders in women in reproductive age. As for the treatment of this disease the lack of a clear etiology for PCOS has led to a symptom-orientated treatment. Howe-ver, the overall aims of treatment are to induce ovulation for women desiring conception, to reduce androgen levels, to reduce body weight and to reduce long-term health risks of diabetes mellitus and cardiovascular disease. Clomiphe-ne citrate (CC) is recommended as first line treatment for induction of ovulation in patients with PCOS by virtue of its efficacy, safety, and ease of administration. Alternatives for CC-resistant patients include gonadotrophin therapy (better with low-dose step-up protocol) and laparoscopic ovarian diathermy. Recently, recombinant FSH (rFSH) has been introduced in clinical practice and it seems more effective than urinary FSH as demonstrated by a significantly higher number of follicles recruited and embryos obtained with a shorter treatment period. The addition of GnRH-agonist to the stimulation protocol for women affected by PCOS could reduce premature luteinization and increase cycle fecundity. Other drugs under investigation are metformin and cabergoline. Hirsutism is the manifestation of hyperandrogenemia in PCOS. The primary goal of the treatment of hirsutim is central or peripheral androgen suppression using 3 groups of drugs: inhibitors of androgen production (oral contraceptives, GnRH analogues), peripheral androgen blockers (cyproterone acetate, flutamide, finasteride and spironolactone), and insulin-sensitizing agents (metformin). Weight reduction and exercise could also improve not only menstrual disturbances and infertility, but also insulin resistance and its adverse metabolic con-sequences.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=14973407&dopt=Abstract [PubMed - in process]
Minerva Ginecol. 2004 Feb;56(1):63-79.
Metformin for the treatment of the polycystic ovary syndrome.
Barbieri RL, Gargiulo AR.
Department of Obstetrics, Gynecology and Reproductive Biology, Brigham and Women's Hospital, Boston, MA, USA.
The polycystic ovary syndrome (PCOS) is characterized by increased secretion of LH, insulin and androgens. The main clinical complaints of women with PCOS include: oligo- or amenorrhea, dysfunctional uterine bleeding, hirsutism, obesity and/or anovulatory infertility. The first line treatment for these problems include: 1) estrogen-progestin therapy for oligomenorrhea and dysfunctional uterine bleeding; 2) estrogen-progestin therapy and/or antiandrogens for hirsutism; 3) lifestyle changes such as diet and exercise for obesity and 4) weight loss or clomiphene for anovulatory infertility. However, clinical trials have indicated that metformin is effective second line therapy when first line therapy has not been effective, is not acceptable to the patient or is medically contraindicated. The addition of metformin to the armamentarium of the gynecological endocrinologist represents an important advance.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=14973411&dopt=Abstract [PubMed - in process]
Diabete Metab. 1991 May;17(1 Pt 2):180-4.
Glucose and lipid metabolism in non-insulin-dependent diabetes. Effect of metformin.
Riccio A, Del Prato S, Vigili de Kreutzenberg S, Tiengo A.
Cattedra di Malattie del Ricambio, University of Padova, Italy.
Basal and insulin-mediated glucose and free-fatty acid (FFA) metabolism was evaluated in 6 non-insulin-dependent diabetic patients (NIDDM) previously treated by diet, before and after 4 week metformin treatment (850 mg twice/day). On both occasions, an euglycemic stepwise insulin (20 and 40 mU/m2/min) clamp was performed along with primed-continuous infusion of 3-3H-glucose and 1-14C-palmitate and indirect calorimetry monitoring. FFA oxidation rate was measured from the rate of appearance of 14CO2. After metformin therapy, fasting plasma glucose, FFA, triglyceride, total cholesterol concentrations and HbA1c were all lowered (p less than 0.05-0.01) in the absence of any change in plasma insulin levels. Plasma FFA turnover rate (5.3 +/- 0.5 vs 3.9 +/- 0.8 mumol/kg/min; p less than 0.05) and FFA oxidation (0.93 +/- 0.12 vs 0.70 +/- 0.12 mumol/kg/min; p less than 0.05) were also lower after metformin treatment, while glucose oxidation increased from 0.9 +/- 0.2 vs 1.2 +/- 0.1 mg/kg/min. During the insulin clamp studies, whole body glucose disposal was higher both at the lower (2.1 +/- 0.4 vs 2.8 +/- 0.4 mg/kg/min) and higher insulin plateau (4.8 +/- 0.9 vs 6.3 +/- 0.9 mg/kg/min; p less than 0.01). Since no difference was apparent in glucose oxidation, the increase in glucose disposal was entirely accounted for by an improvement in non-oxidative glucose metabolism. Euglycemic hyperinsulinemia was followed by a reduction in plasma FFA concentration turnover rate that remained the same before and after metformin therapy. In conclusion, metformin treatment induces an improvement in glucose metabolism both in the basal and insulin-stimulated state.(ABSTRACT TRUNCATED AT 250 WORDS)
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1936473&dopt=Abstract
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