Sandy presented her findings at the ENSA Scientific Meeting in Melbourne last year and was awarded a travel grant to allow her to attend and present at the US Endocrine Society meeting in Washington DC this year.  She also won an award for the best new presenter at the meeting.  Sandy showed that men who have infertility as a result of a pituitary gland insufficiency can successfully achieve fatherhood with medical treatment, without the need for the partner to undergo IVF.  Sandy’s research highlighted the central role of the specialist endocrine nurse in a fertility clinic. Her attendance at the US meeting will allow her to exchange information with endocrine nurses from around the world.

The Keogh Institute has an active clinic treating men with endocrine disorders which affect their sperm count and their fertility.  Sandy van der Westhuizen is the endocrine nurse in charge of the fertility service.

The clinic number is 9346 2008

The serendipitous discovery that a drug, originally developed for cardiovascular use, restored erectile function has led to a burgeoning of research into the link between erectile function and cardiovascular health.

Our audit of the screening biochemistry of 1500 men presenting to the Keogh Institute with erectile dysfunction (ED) has shown that dyslipidaemia is by far the most prevalent abnormality, far more common than a low testosterone. Prevalence studies led by Dr Kim Chew in Western Australian general practice and in the community have confirmed that men with ED are at high odds of having cardiovascular disease and vice versa.

The big question has been whether ED by itself is an independent sign of underlying cardiovascular disease. Our clinical laboratory experiments, using measures of endothelial function in conduit and resistance arteries in the forearm, have suggested that this is so. Men with ED, without any known cardiovascular disease or any measurable cardiovascular risk factors were found to have demonstrable generalised vascular disease. This finding is consistent with the “artery size” hypothesis where endothelial dysfunction and disease presents first in small arteries, such as in the penis, causing ED, before being clinically evident in larger diameter arteries like the coronary circulation, causing angina or myocardial infarction. Presently, using data from our own clinic and the WA Morbidity and Mortality Database we are examining the time interval between those two events. We believe that this time interval represents a window of opportunity for cardiovascular risk reduction.

The prime focus of the management of ED has now moved from psychological counselling to identification and correction of cardiovascular risk factors.

ED is not the only men’s health issue moving from the psychological to the organic sphere of interest. Premature ejaculation (PE) is said to the most common male sexual complaint and is divisible into primary PE, which occurs and persists from the first sexual encounter, and secondary or acquired PE, which may be psychological but is commonly acquired in the older patient when erectile function begins to fail. Primary PE is now recognised to have an organic, probably genetic, basis although the exact mechanisms by which it occurs are yet to be fully elucidated. PE has been previously managed, rather unsuccessfully, by psychological and behavioural interventions. However, the recognition of the role of serotonin receptors in the control of ejaculation has led to the use of selective serotonin reuptake inhibitors and the development of newer SSRIs in the management of primary PE. However there is more to unravel in the complex imbalance in neurotransmitters and autonomic nervous control which leads to primary PE and, led by Dr Neil Palmer, the Keogh Institute is taking PE from the examination couch back to the clinical laboratory.

BACKGROUND: Polycystic ovary syndrome (PCOS) is associated with insulin resistance and features in common with the metabolic syndrome (MetS)—factors shown to predict cardiovascular risk and type 2 diabetes. We investigated the prevalence and characteristics of the MetS in PCOS by three definitions—World Health Organization (WHO), National Cholesterol Education Program Adult Treatment Panel III (NCEP-ATP-III) and International Diabetes Federation (IDF)—and compared that with the background population. 

METHODS: Cross-sectional study of 168 women with PCOS and 883 age-matched controls from the Australian Diabetes, Obesity and Lifestyle (AusDiab) study. 

RESULTS: Prevalence of the MetS in PCOS subjects was 33% by WHO, 37% by NCEP-ATP-III and 40% by IDF criteria, compared with 10% by NCEP-ATP-III and 13% by IDF in controls (P < 0.001). MetS by WHO criteria was not calculated in the AusDiab population. Age was an independent predictor of MetS in PCOS and controls. The prevalence of MetS was significantly higher among those with PCOS (P 5 0.027) in obese women (BMI > 30 kg/m2), and higher but not significantly so in overweight (BMI 25–30 kg/m2) women (P = 0.052). Dehydroepiandrosterone sulphate was associated with a lower risk of the MetS—Odds ratio 0.86 (95% confidence interval, 0.77–0.97, P 5 0.011). 

CONCLUSIONS: An approximate 4-fold increase in the prevalence of the MetS in women with PCOS compared with the general population, consistent with the proposed major role of insulin and obesity in the syndrome, implies greater risk of cardiometabolic disease in women with PCOS. However, this estimate is likely to vary according to PCOS definition, ethnicity and different aetiological pathways to PCOS.

Annals of Internal Medicine, 148:569-577, 2008.

Menopause, 15(6):1065-1069, 2008.

Medical Journal of Australia, 189(5): 250-253, 2008.

Journal of Sexual Medicine, doi: 10.1111/j.1743-6109.2008.00971.x, 2008.

Bone, 42(6):1219–1225, 2008.

Diabetes Care, 31(8):1502-9, 2008.

Journal of Sexual Medicine, 5(10):2282-2290, 2008.