Stella R. Milsom
University of Auckland
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Publication
Featured researches published by Stella R. Milsom.
Australian & New Zealand Journal of Obstetrics & Gynaecology | 2001
Karen Williamson; Alistair J. Gunn; Neil Johnson; Stella R. Milsom
Summary: The effect of etnnicity on me prevalence ana presentation of polycystic ovarian syndrome (PCOS) was examined in a cross‐sectional study of women with clinical ‐ and ultrasound ‐ diagnosed PCOS. European, Maori and Pacific Island women were seen in proportion to the general population, whereas Indian women were over‐represented and Chinese women under‐represented. European and Maori women were more likely to present with hirsutism than other ethnic groups (43% versus 25%, p < 0.05), while European women were less likely to present with infertility (46% versus 68%, p < 0.01). The Pacific Island women had little or no acne but other signs of PCOS were similar among ethnic groups. Although less than 10% of patients were referred with obesity, the majority of PCOS women were overweight on examination. Maori and Pacific Island women were more obese and had the highest rates of insulin resistance and lipid abnormalities. The adverse metabolic profile of many of these women, particularly the Maori and Pacific Islanders, is very likely to predispose them to early cardiovascular disease.
Hormone Research in Paediatrics | 2008
Stella R. Milsom; Werner F. Blum; Alistair J. Gunn
Aim: To evaluate the postpartum time course of changes in insulin-like growth factors (IGFs) and their binding proteins (IGFBPs). Methods: Breast milk IGF-I and IGF-II and IGFBP-1, IGFBP-2, and IGFBP-3 levels were determined in 23 women with babies born at term, from day 4 until up to 9 months after birth. Results: The IGFBP-3 levels were highest from day 4 to day 6 and then decreased by days 10–12. In contrast, IGF-I and IGF-II and IGFBP-1 and IGFBP-2 showed little change over the first 2 weeks after birth. Subsequently, all the IGF components showed a moderate decline over approximately the first 1–3 months and then stable levels up to 9 months after birth. Conclusion: Although the possibility cannot be excluded that these changes in levels of IGFs and their binding proteins in human milk represent passive loss from the mammary gland, we speculate that higher early levels of the human milk IGF system contribute to maturation of the infant gut.
Hormone Research in Paediatrics | 1998
Stella R. Milsom; Diana L. Rabone; Alistair J. Gunn; Peter D. Gluckman
In order to evaluate the galactopoietic response to rhGH in mothers of normal babies with idiopathic lactation insufficiency arising in the early postpartum period, we performed a preliminary, randomised, single blind trial of 3 different doses of hGH: either 0.05, 0.1, or 0.2 IU/kg/day to a maximum of 16 IU/day, for 7 days. Total 24-hour milk production was determined in each mother 1 day prior to initiating therapy and on the last day of therapy. Milk production rose by 36.0 ± 12.6% in the group receiving 0.2 IU/kg/day (n = 6) but by only 4.7 ± 9.7%, (p < 0.04) in the combined lower dose group (n = 10). In conclusion, these data suggest that moderate dose hGH therapy in mothers with lactation insufficiency can improve galactopoiesis.
British Journal of Obstetrics and Gynaecology | 2003
Stella R. Milsom; Martin C. Sowter; Marion A. Carter; Bruce S. Knox; Alistair J. Gunn
Objective To determine whether using newer monoclonal rather than polyclonal assays for measuring luteinising hormone (LH) alters the predictive value of LH and LH/follicle‐stimulating hormone (FSH) ratios for polycystic ovarian syndrome.
Australian & New Zealand Journal of Obstetrics & Gynaecology | 2002
Stella R. Milsom; Gillian Gibson; Karen Buckingham; Alistair J. Gunn
The present study was designed to determine whether clinical and endocrine characteristics assessed on initial screening of normogonadotropic oligo/amenorrhoeic infertile patients could predict ovulation and then conception and successful live birth or miscarriage.
Australian & New Zealand Journal of Obstetrics & Gynaecology | 2012
Stella R. Milsom; Kate Duggan; Susannah O'sullivan; Megan Ogilvie; Alistair J. Gunn
Infertility in idiopathic or acquired hypogonadotropic hypogonadism (HH) was managed with exogenous gonadotropins and artificial reproduction as needed, in Auckland, New Zealand, from 2000 to 2010. Of eight men seeking conception, 2/2 with acquired HH but only 2/6 with congenital HH achieved clinical pregnancy with exogenous gonadotropins, whereas 12/14 women (86%) achieved one or more live births. Current gonadotropin treatment does not seem to be optimal for men with congenital HH.
Internal Medicine Journal | 2011
Cara M. Ogilvie; Stella R. Milsom
Dopamine agonist therapy has been the cornerstone treatment for prolactinoma since the 1970s, replacing surgery in the primary management of this condition. These agents are effective in the management of prolactin excess, have a low side‐effect profile, and in some cases may even be curative. However, recent studies of high dose dopamine agonists used in Parkinsons disease have raised the possibility that these drugs may be associated with cardiac valvulopathy. This paper discusses the modern use of dopamine agonists in a patient with prolactinoma.
Fertility and Sterility | 2008
Sasha Nair; Stella R. Milsom
OBJECTIVE To describe the resolution of anejaculation associated with PRL excess by dopamine agonist treatment. DESIGN Case report. SETTING Fertility clinic. PATIENT(S) Two men with anejaculation, in one case with associated infertility. INTERVENTION(S) Dopamine agonist treatment. MAIN OUTCOME MEASURE(S) Resolution of anejaculation and infertility. RESULT(S) Endocrine investigations in both men revealed low serum T, elevated PRL, and a pituitary microadenoma. Treatment with a dopamine agonist normalized serum hormone profiles and restored sexual function, with subsequent involution of the adenoma. CONCLUSION(S) Prolactinoma manifesting as anejaculation is rare but responds readily to treatment with a dopamine agonist. Serum PRL should be measured in any man presenting with anejaculation.
British Journal of Obstetrics and Gynaecology | 2005
Megan Ogilvie; James S. Davidson; Phillipa Cuttance; Stella R. Milsom
A 34 year old school principal developed virilising symptoms at 35 weeks of gestation in her second pregnancy. Her menses had been regular but mild hirsutism and acne had been present since age 20 years. Her first child had been conceived at age 29, one year after stopping contraception. Mild acne and hirsutism had been noted at 16 weeks of gestation, and became more severe at 30 weeks of gestation, temporally associated with dexamethasone therapy for threatened early labour. Ultrasound scanning at 36 weeks had shown two solid homogeneous masses in the abdomen. The left measured 106 mL and the right 157 mL. She was induced at 37 weeks of gestation following signs of eclampsia and delivered a phenotypically normal male child. Postpartum maternal examination revealed significant hirsutism (Ferriman-Gallwey score 34/48) and cystic acne involving the face, trunk, and upper arms. Pelvic computed tomography was unremarkable postpartum and androgenic hormone measurements were in the normal range: testosterone <1 nmol/L, DHEAS 2.2 Amol/L, androstenedione 3.4 nmol/L, 17-hydroxyprogesterone 0.7 nmol/L. A combined anti-androgen–oestrogen oral contraceptive was prescribed (ethinylestradiol 35 Ag/ cyproterone acetate 2mg), but was subsequently discontinued. There was spontaneous return of menses and resolution of her acne and hirsutism over the next 12 months. She conceived her second pregnancy aged 34 years and reported acne, hirsutism, lowering of her voice, and significant weight gain from 12 weeks of gestation. She was shaving facial hair twice daily and teaching had been become an embarrassment. Examination revealed significant virilisation with a FG score of 33, clitoromegaly of 2 cm, grade 4 acne on face, chest and back, and a deep voice. Her facial appearance was masculine. She was referred to our unit at 35 weeks for management. Endocrine data from this pregnancy are presented in Table 1, confirming extreme hyperandrogenism. Ultrasound at 34 weeks demonstrated a male fetus and bilateral solid ovarian masses, size not able to be determined due to the presence of the pregnant uterus. A decision was made to proceed with the pregnancy until fetal viability was assured, given the presence of a male fetus and the expectation that the underlying pathology was likely to be benign. By 36 weeks of gestation, maternal symptoms were so marked, however, that labour was induced and she was delivered of a healthy male infant, confirmed to have an XY karyotype. Magnetic resonance imaging two weeks postpartum revealed ovarian enlargement (36 mL bilaterally) but no masses or cysts, and androgen levels normalised within two weeks of delivery. Following a brief period of lactation, a Mirena IUD was inserted and sequential cyproterone was administered in a dose of 100 mg for 10 days per month, with gradual amelioration of her acne and hirsutes in the six months post-delivery. Ultrasound of the pelvis at three months postpartum demonstrated ovaries of normal volume (8 mL bilaterally) with no morphological evidence of polycystic ovarian syndrome. The presumptive diagnosis was recurrent bilateral luteoma.
Australian & New Zealand Journal of Obstetrics & Gynaecology | 2009
Cara M. Ogilvie; Rhona Levenberg; Stella R. Milsom
1 Leung AKC, Robson WLM, Tay-Uyboco J. The incidence of labial fusion in children. J Pediatr Child Health 1993; 29: 235. 2 Acharya N, Mandal AK, Ranjan P, Kamat R, Kumar S, Singh SK. Labial fusion causing pseudoincontinence in an elderly woman. Int J Gynaecol Obstet 2007; 99: 246–247. 3 Papagianni M, Stanhope R. Labial adhesions in a girl with isolated premature thelarche: The importance of estrogenization. J Pediatr Adolesc Gynecol 2003; 16: 31–32. 4 Davis VJ, Coates M. Success of medical management of labial adhesions. J Pediatr Adolesc Gynecol 2001; 14: 142. 5 Nurzia JM, Eickhorst KM, Ankem MK, Barone JG. The surgical treatment of labial adhesions in pre-pubertal girls. J Pediatr Adolesc Gynecol 2003; 16: 21–23.