Search PubMed⌕ Search

Biomedical subjects

S Franks

Publications and source records attributed to S Franks.

194 records · Page 11Linked to original sources
PubMed1975

Therapy-orientated diagnosis of secondary amenorrhoea.

A programme for investigation of secondary amenorrhoea is described, which is based upon a functional classification of the endocrine causes of anovulation. All diagnostic enquiries not directly yielding a therapeutic dividend are excluded from this protocol. Three main categories of amenorrhoea are recognised: primary ovarian disease, hyperprolactinaemia and disorders of gonadotrophin secretion. There are subdivisions of each category, each with its own special diagnostic and therapeutic implications. Initial investigations take 6 weeks to complete and include measurements of follicle-stimulating hormone and prolactin, pituitary radiology and assessment of oestrogen production and of the response to clomiphene. The results of analysis of 75 consecutive cases of amenorrhoea and of 18 patients treated for infertility are presented and a cost benefit analysis applied.

Amenorrhea↗
PubMed1974

Prolactin concentrations in patients with breast cancer.

Basal prolactin levels were measured before operation in 113 patients undergoing surgery for a lump in the breast. Prolactin concentrations were not significantly higher in those patients with breast cancer than in those with benign lumps. Prolactin concentrations were, however, found to be higher in premenopausal women than in postmenopausal ones, regardless of tumour histology.

Adenofibroma↗
PubMedDate not supplied

Etiology of anovulation in polycystic ovary syndrome.

Various endocrine factors may contribute to the phenomenon of arrested follicular development, which is the hallmark of anovulatory infertility in polycystic ovary syndrome. Hypersecretion of luteinizing hormone and/or insulin, together with high intrafollicular concentrations of androgens, can interact to produce supraphysiological levels of cyclic AMP in granulosa cells, resulting in premature activation of terminal differentiation and, hence, arrest of follicle growth.

Anovulation↗
PubMedDate not supplied

Multifollicular ovaries: clinical and endocrine features and response to pulsatile gonadotropin releasing hormone.

By means of pelvic ultrasonography, a multifollicular ovarian appearance was observed in women with weight-loss-related amenorrhoea. Multifollicular ovaries (MFO) are normal in size or slightly enlarged and filled by six or more cysts 4-10 mm in diameter; in contrast to women with polycystic ovaries (PCO), stroma is not increased. Unlike PCO patients, women with MFO were not hirsute and serum concentrations of luteinising hormone and follicle stimulating hormone were normal and decreased, respectively. The uterus was small indicating oestrogen deficiency. In MFO, treatment with gonadotropin releasing hormone (LHRH) induced ovulation in 83% of cycles and there were seven pregnancies in 8 women; in PCO, only 40% of cycles were ovulatory and there were eleven pregnancies (8 women) but six of these aborted. In MFO ovarian morphology reverted to normal in ovulatory cycles, whereas in PCO the polycystic pattern persisted despite the presence of a dominant follicle. MFO may represent a normal ovarian response to weight-related hypothalamic disturbance of gonadotropin control.

Amenorrhea↗
PubMedDate not supplied

Polycystic ovary syndrome: evidence for a primary disorder of ovarian steroidogenesis.

Polycystic ovary syndrome (PCOS) is a very common endocrinopathy of uncertain aetiology in which the most consistent biochemical abnormality is hypersecretion of androgens. In this review, evidence is presented to support the view that a primary abnormality of ovarian androgen biosynthesis provides the basis for the syndrome. PCOS is a familiar disorder and we demonstrate, in molecular genetic studies, that CYP11a, the gene coding for P450 side chain cleavage, is a key susceptibility locus for development of hyperandrogenism.

Androgens↗
PubMedDate not supplied

Modern use of clomiphene citrate in induction of ovulation.

Clomiphene citrate is the treatment of first choice in the management of infertility in normally oestrogenized, anovulatory women (WHO group II). The majority of women with 'pure' anovulatory infertility respond to treatment with clomiphene citrate. The rates of pregnancy and miscarriage are close to those expected in a normal fertile population. Basal hormone concentrations do not predict outcome. An increased body mass index is the only factor which is consistently associated with a decreased response to clomiphene citrate; it follows therefore, that weight reduction should be an important part of therapy in anovulatory women. According to our data, only an increased luteinizing hormone value immediately post clomiphene citrate predicted an adverse pregnancy outcome in women who conceived. Clomiphene citrate, along with other ovulation induction therapies, can cause multiple follicular development, with a risk of ovarian hyperstimulation and multiple pregnancy. Ultrasound monitoring of treatment is important in order to choose the appropriate dose of clomiphene citrate in subsequent cycles and to minimize the risks of hyperstimulation and multiple pregnancy. When couples with other factors contributing to subfertility are excluded, the cumulative conception rate continues to rise after 6 months of treatment with clomiphene citrate, reaches a plateau by treatment cycle 12 and approaches that of the normal population. It has been reported that prolonged use of clomiphene citrate may be associated with an increased risk of a borderline or invasive ovarian tumour. Taking into consideration these observations, we recommend that anovulatory women responsive to clomiphene citrate should be treated for at least 6 cycles before considering more complex or invasive methods of ovulation induction, and that treatment should probably be limited to a maximum of 12 cycles.

Adult↗
PubMedDate not supplied

Candidate genes in polycystic ovary syndrome.

The candidate gene approach has already paid some dividends in trying to understand the complex genetics of polycystic ovary syndrome (PCOS). In terms of steroidogenic abnormalities, CYP11a-encoding P450 side chain cleavage-appears to be a major susceptibility locus. In relation to the well-described metabolic disturbances in PCOS, the insulin gene variable number tandem repeat (VNTR) appears to be a promising candidate, at least in populations studied in the UK. Finally, genes implicated in ovarian follicular development may have a role in the aetiology of PCOS, as demonstrated by recent identification of the follistatin gene as a potential disease locus. It seems unlikely that PCOS can be explained on the basis of a single gene disorder although, in a given family, one gene may have a predominant effect. An oligogenic model seems the most appropriate basis on which to understand the genetic origins of this very common disorder. The candidate gene approach has been useful to date, but it may prove important in the near future to perform an anonymous genome-wide scan to identify hitherto unheralded susceptibility loci.

Activins↗