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Hum Fertil (Camb). 2000;3(2):106-111.
Ovulation induction for polycystic ovary syndrome.

Balen A.

Department of Reproductive Medicine, The General Infirmary, Leeds LS2 9NS, UK.

Polycystic ovary syndrome (PCOS) is the commonest cause of anovulatory infertility. Various factors influence ovarian function, and fertility is adversely affected by an individual being overweight or having high serum concentrations of LH. Strategies to induce ovulation include weight loss, oral anti-oestrogens (principally clomiphene citrate), parenteral gonadotrophin therapy and laparoscopic ovarian surgery. There have been no adequately powered randomized studies to determine which of these therapies provides the best overall chance of an ongoing pregnancy. Women with PCOS are at risk of ovarian hyperstimulation syndrome (OHSS) and so ovulation induction has to be monitored carefully with serial ultrasound scans. The recognition of an association between hyperinsulinaemia and PCOS has resulted in the use of insulin sensitizing agents, such as metformin, which appear to ameliorate the biochemical profile and improve reproductive function.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11844364&dopt=Abstract [PubMed - as supplied by publisher]




Hum Fertil (Camb). 2000;3(2):93-95.
Hyperinsulinaemia and polycystic ovary syndrome.

Conway GS.

Cobbold Laboratories, The Middlesex Hospital, Mortimer Street, London W1N 8AA, UK.

Over the past 20 years, it has been established that hyperinsulinaemia is a fundamental disturbance in many women with polycystic ovary syndrome (PCOS). A subgroup of women with this syndrome have 'metabolic PCOS' which can be considered to be a pre-diabetic state. Clinically, this subgroup is most easily identified in obese women with a strong family history of diabetes in whom menstrual disturbance is the predominant feature. There is an urgent need to define the more subtle features in young lean women with PCOS, in whom the metabolic syndrome is yet to emerge, which would enable the prediction of future health risks. The molecular mechanisms of insulin resistance leading to hyperinsulinaemia are now being elucidated. Abnormalities of both insulin secretion and intracellular insulin signalling have both been proposed in women with PCOS. Strategies to lower serum insulin concentrations include diet, exercise and possibly, oral insulin sensitizing agents such as metformin. Although the short-term efficacy of reducing hyperinsulinaemia in women with PCOS is clear, the best method to prevent the progression to diabetes later in life has not been defined.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11844361&dopt=Abstract [PubMed - as supplied by publisher]




Metabolism. 1994 May;43(5):647-54.
Metformin therapy in polycystic ovary syndrome reduces hyperinsulinemia, insulin resistance, hyperandrogenemia, and systolic blood pressure, while facilitating normal menses and pregnancy.

Velazquez EM, Mendoza S, Hamer T, Sosa F, Glueck CJ.

University of the Andes, Merida, Venezuela.

Using polycystic ovary syndrome (PCOS) as a model of insulin resistance and hyperandrogenism, our specific aim was to assess the effect of Metformin on lipoproteins, sex hormones, gonadotropins, and blood pressure in 26 women with PCOS who were studied at baseline, received Metformin 1.5 g/d for 8 weeks, and were then restudied. None of the women had normal menstrual cycles, 100% had multiple subcapsular follicules by pelvic ultrasound, 90% were hirsute, and 85% had high free testosterone. Comparing post-Metformin versus baseline levels, the Quetelet Index (QI) decreased 1.5% (P = .04) and the waist to hip ratio (WHR) decreased 2.8% (P = .003). After covariance adjusting for changes in the QI and WHR, on Metformin the area under the insulin curve (IA) during oral glucose tolerance testing decreased 35% (P = .04), and the insulin area to glucose area ratio decreased 31% (P = .03). On Metformin, covariance-adjusted systolic blood pressure (SBP) decreased (P = .04) and apo A-1 increased (P = .05). On Metformin, with improvement in insulin sensitivity, there were sharp reductions in covariance-adjusted luteinizing hormone ([LH] P = .0007), total testosterone ([T] P = .0004), free T (P = .0001), androstenedione (P = .002), dehydroepiandrosterone sulfate ([DHEAS] P = .006), and the free androgen index ([FAI] P = .0005), with increments in follicle-stimulating hormone ([FSH] P = .04) and sex hormone-binding globulin ([SHBG] P = .04).(ABSTRACT TRUNCATED AT 250 WORDS)

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8177055&dopt=Abstract












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