BACKGROUNDThere is a need for an easily accessible biomarker of sympathetic nervous activation in essential hypertension, but none exists. Heart rate (HR) has been suggested, but requires validation, now doubly important as an elevated HR in hypertension has emerged as an independent cardiovascular risk factor.METHODSIsotope dilution methodology was used to measure total and regional noradrenaline spillover and adrenaline secretion rates in 30 patients with unmedicated essential hypertension and in a comparator group of 48 healthy participants with normal blood pressure. The particular interest was in the relationship of measured HR to cardiac noradrenaline spillover, the measure of cardiac sympathetic activity.RESULTSSympathetic activation was present in the patients with essential hypertension, evident in significantly increased mean cardiac, renal and total noradrenaline spillover rates. Adrenaline secretion was normal. HR in hypertension correlated directly with cardiac noradrenaline spillover (r = 0.82, P = 9.3 × 10), but not with renal noradrenaline spillover or adrenaline secretion. 67% of the variance in HR was attributable to differences in cardiac sympathetic activity. Among hypertensive patients there was no internal correlation between cardiac noradrenaline spillover, renal noradrenaline spillover and adrenaline secretion; the sympathetic activation commonly was not 'global'. In healthy participants HR did not correlate with measures of sympathetic activity or adrenaline secretion.CONCLUSIONWhen sympathetic activation exists in essential hypertension it is differentiated, not necessarily involving all sympathetic outflows. An elevated HR proved to be a biomarker of cardiac sympathetic activation but not activation of the renal sympathetic outflow. Identifying activation of the cardiac sympathetic outflow as the prime mechanism of hypertension tachycardia is relevant to therapies which should now be considered to minimize cardiovascular risk in this clinical setting. Is an elevated HR a valid biomarker of sympathetic activation in essential hypertension? Yes, but only for the cardiac sympathetic outflow. The unavoidable principle is that regional differentiation of sympathetic responses in essential hypertension means that no simple test can ever represent each and every sympathetic outflow.

Unlike noradrenaline, the sympathetic neurotransmitter which overflows to the circulation, adrenaline (ADR) is a secreted hormone, with a low plasma concentration, and plasma concentration for biological action a log order lower than that of noradrenaline. The venous drainage of the left adrenal medulla into the left renal vein does expose this vein to uniquely high plasma ADR concentrations and possible risk of thrombosis at high rates of ADR secretion. There is typically a different timeframe for adrenal medullary and sympathetic nervous system responses: ADR release is short term in contrast with sympathetic activation persisting for years in heart failure and hypertension. The historic view of Walter Cannon, subject to recent review, that the sympathoadrenal system is a unified biological system, was deconstructed further with demonstration of frequent mismatching of adrenal medullary and sympathetic nervous responses. Under gravity stimulation with standing, there is prompt sympathetic activation without ADR release. In many diseases, notably obesity, hypertension, heart failure and depressive illness, an activated sympathetic nervous system and silent adrenal medulla coexist. The therapeutic corollary of this is that ADR blockade is much less commonly needed clinically than pharmacological antagonism of the sympathetic nervous system.

In our recent short report [1], we suggested that angiotensin receptor blocking drug (ARB) prescribing in hypertension may possibly be adverse, because this drug class can increase angiotensin-converting enzyme-2 (ACE2) expression, this protein being the molecular latch for SARS-CoV-2 virus entry to cells in COVID-19 infections. We also suggested, more generally, that reducing ACE2 expression could be a therapeutic principle for COVID-19 control. We now welcome medical letters from four correspondents. One, Dr Ekan Cüre [2] extends the case for possible pharmaceutical hazard in COVID-19, providing evidence that actually some drugs additional to those initially suspected increase membrane ACE2 expression. The other three correspondents, Paolo Verdecchia [3], Francisco Jose Fernandez-Fernandez [4] and Liu and colleagues [5], take a different tack. They suggest that increasing the expression of ACE2 in the lungs can be beneficial in acute respiratory disease syndrome (ARDS), including perhaps that due to COVID-19. Accordingly, pharmacologically inducing increased pulmonary ACE2 with renin-angiotensin system blockers might be helpful in COVID-19. DOES INCREASED ACE2 EXPRESSION MATTER? Several types of experiment in animals give credence to the idea that the level of human ACE2 expression may perhaps be important in COVID-19 infection. Knockout mice genetically modified to have no ACE2 are totally resistant to coronavirus infections [6]. There is a converse to this. In two studies, transgenic mice were bred to overexpress human ACE2 [7,8]. These hACE2 transgenic mice demonstrated markedly increased infectivity and lethality when exposed to SARS coronavirus. Despite this type of evidence, it is commonly said that with ARB and ACE-inhibitor dosing in humans, the induction of ACE2 would be insufficient to matter, and anyway, may not be in the lungs. But this criticism can be discounted applying a body of relevant evidence, both experimental and clinical (described in more detail below), deriving from studies in which ARB and ACE-inhibitor dosing has been used to replenish ACE2 in the lungs in lung failure syndromes resulting from influenza virus, acid inhalation and other noxious influences [6,9–11]. Pulmonary ACE2 expression is demonstrably increased by renin-angiotensin block in this context, with strong evidence that it improves survival [6,9–11]. In short, the drugs in question for our hypothesis do induce increased pulmonary ACE2 expression, which has biological benefit in noncoronavirus ARSD. With coronavirus exposure it is plausible to ask, as we do, whether the biological effect of drug-induced pulmonary ACE2 expression may be deleterious, promoting infectivity and lethality. PHARMACOLOGICAL AND OTHER MECHANISMS WHICH INCREASE ACE2 EXPRESSION Cüre and Cumhur Cüre [2] importantly extend the spectre of possible pharmaceutical hazard in COVID-19 by providing evidence that statins, specifically rosuvastatin [12] and some antidiabetic drugs, possibly sodium-glucose transporter protein 2 (SGLT2) inhibitors [13] and certainly glucagon-like peptide-1 receptor (GLP-1) agonists [14] increase membrane ACE2 expression. In our hypothesis [1], we were circumscribed and specific, focusing on ARBs and hypertension. Cüre and Cumhur Cüre demonstrate that there may be a need to think more broadly on this matter. He has extended the issue to prescribing of statins and antidiabetics. How these drugs increase ACE2 expression is unclear. For other drugs that influence ACE2 expression, their action on body sodium balance appears to be a common link, with sodium depletion elevating ACE2. ARBs, and less consistently ACE-inhibitors, increase ACE2 expression, and decrease body sodium content [1]. Aldosterone reduces ACE2 expression [15], mineralocorticoid block with spironolactone increases expression [16]. We suggested [1] that elevated plasma angiotensin, a substrate of ACE2, which is elevated by ARBs and accompanies sodium depletion in general, may regulate the expression of the linked enzyme, ACE2. Things turn out not to be as simple as that, which may partly explain why ACE-inhibition, which reduces body sodium, but through a direct action lowers plasma angiotensin, elevates ACE2 less consistently than ARBs. Much as for aldosterone dosing, dietary sodium loading reduces ACE2 expression [17]. This effect of sodium ingestion is relevant to the use of proximal small intestine tissue, accessed by endoscopic biopsy, used in direct studies of human ACE2 [18]. Direct exposure of the duodenum to sodium in a meal could be a confounder. PULMONARY ACE2 IN SEVERE LUNG INJURY: A POTENTIAL THERAPEUTIC TARGET? Three of the correspondents, Verdecchio et al. [3], Fernandez-Fernandez [4] and Liu and colleagues [5], develop the case, which was first presented in relation to the SARS epidemic [6], which in severe lung injury pulmonary ACE2 is depleted. A special form of this pulmonary ACE2 depletion is seen with coronavirus infections, wherein after the virus binds to the ACE2 protein both are internalized, depleting membrane ACE2 [6]. Depletion of ACE2 is accompanied by accumulation of angiotensin, its substrate, in the lung, with adverse effects. The plasma concentration of angiotensin does rise substantially in severe COVID-19 infections [19]. There is a body of experimental and clinical evidence, mentioned above, that renin-angiotensin block, by repleting ACE2, is beneficial in noncoronavirus ARDS, caused by influenza viruses, acid inhalation and other noxious influences [6,9–11]. Could this benefit extend to COVID-19 infection? A trial of the ARB losartan in severe COVID-19 infections, based on this line of thinking, has commenced (ClinicalTrials.gov Identifier: NCT04312009). Such a trial may carry risks of worsening the infection. Benefit from renin-angiotensin system block in acute severe lung disease has not been shown experimentally in coronavirus infections. Augmenting pulmonary ACE2 expression might increase coronavirus uptake and viral load. The classic study of Kuba et al.[6] is often misquoted as providing evidence of ARBs and ACE-inhibitors benefiting coronavirus pneumonia. Kuba et al.[6] actually administered coronavirus fragments, spike protein, not replicable entire virus. The spike fragments depleted pulmonary ACE2 after binding, aggravating the existing experimental pneumonia, which was improved by pharmacological renin-angiotensin system block. Neither this study, or any others to our knowledge, have demonstrated benefit of renin-angiotensin block in coronavirus infection. The transgenic experimental animals overexpressing hACE2 mentioned above previously were demonstrated to have increased infectivity and lethality with SAR coronavirus [7,8]. Augmentation of virus uptake and replication presumably overwhelmed any specific pulmonary benefits. TESTING OF THE HYPOTHESIS Hypotheses are made for testing, and for the hypothesis that some common drugs induce ACE2 overexpression and may be adverse in the COVID-19 pandemic, this testing is urgently required. The most immediate and direct clinical testing should come from interrogating the pandemic databases of China and Lombardy. From these populations, presence of COVID-19 illness, illness severity and death could be matched against, age, preexisting medical diagnoses and drugs prescribed at the onset of COVID-19 illness. The multivariate analyses will not be straightforward. There will be a need to differentiate between any effects of ageing, effects of diseases with increased prevalence accompanying ageing (including hypertension, heart failure and diabetes) and the possible effects of drugs given to treat these diseases. Why not test the hypothesis of drug-induced COVID-19 risk in experimental animals? Pretreat the animals with ARBs and ACE-inhibitors to induced overexpressed ACE2, then in a blinded experiment expose the animals to the SARS-CoV-2 virus. But that would not work. Most mammals do not have sufficient structural similarity in their ACE2 protein to human ACE2 to be infected by this virus which is now cursing the human mammal. THE FUTURE It may be difficult to test this hypothesis. Do we as clinicians just live with it, leaving prescribing unchanged? In hypertension, where there are easier alternative prescribing choices, perhaps we can substitute calcium channel blockers and beta-adrenergic blockers for ARBs, and perhaps ACE-inhibitors, if a decision to change antihypertensive medication is made. For chronic renal disease and heart failure, where ARBs and ACE-inhibitors are specifically protective, changes really cannot be recommended, on the basis of a hypothesis. And ‘simply discontinuing medication is strongly discouraged and is not an option’ [1]. Some hypotheses in medicine just fade away. They are a product of their time, have no real importance and no enduring legacy. With this hypothesis for many there is plausibility, and for all such ‘believers’, urgency. What can be the way forward, to prove this hypothesis or refute it? ACKNOWLEDGEMENTS Conflicts of interest There are no conflicts of interest.

The novel coronavirus causing the COVID-19 pandemic, SARS-CoV-2, gains entry to pulmonary cells after binding to membrane ACE2 [1]. This enzyme is a homologue of ACE1, which converts angiotensin I to angiotensin II, is active in cardiovascular control, can be an element in cardiovascular disease, and is therapeutically targeted in hypertension and heart failure, using ACE1 inhibitors such as enalapril and lisinopril. The biology and therapeutic potential of ACE2 is much less clear. Commonly, it is viewed in the cardiovascular sphere as somehow antagonistic to the adverse effects of ACE1, and beneficial. This remains not well worked out, and currently there are no specific cardiovascular therapies involving ACE2. One action of ACE2 is to enzymatically cleave angiotensin II to angiotensin (1–7). Given the importance of ACE2 in SARS-CoV-2 entry to cells, cardiovascular illnesses or cardiovascular drugs, which increase ACE2 expression, and there are several important instances of this [2–6], may perhaps increase human SARS-CoV-2 infectivity and illness severity. We understand that hypertension increases the severity of COVID-19 illness. This is surprising, on two counts. First, ACE2 expression typically is reduced in hypertension models, and second, hypertension does not appear to impact other infections. One of us (M.E.), a cardiologist with more than four decades of hypertension tertiary care experience, cannot recall one of his patients ever dying from an infection. Infection predisposition in diabetes is evident, but not in hypertension. Perhaps in the COVID-19 pandemic, a new infection risk is arising from special properties of some antihypertensive drugs? Angiotensin receptor-blocker (ARB) drugs, now becoming the most commonly used antihypertensive drug class, typically increase ACE2 expression, often very substantially (perhaps two-fold to five-fold) [3–6]. This is sufficiently clear to have sometimes been used in marketing for ARBs, with a claim by pharmaceutical companies that this provides specific benefit in cardiovascular diseases. Perhaps, although this is unproven. With SARS-CoV-2 infection increased ACE2 expression very definitely would not be beneficial, and could be adverse. Increased ACE2 expression with angiotensin receptor blockers has been demonstrated in the kidneys and heart [4–6] but has not been tested to our knowledge, and this is now necessary, in the lungs. Reducing ACE2 expression as a therapeutic principle for COVID-19 control? How might angiotensin receptor blockers increase ACE2 expression. Plasma levels of angiotensin II increase with ARB dosing [7–10]. Angiotensin II is the known substrate for ACE2. Perhaps this is a case of substrate availability increasing the expression of the linked enzyme. This is hypothetical, but could be used as a framework to consider alternative drugs to ARBs during the COVID-19 pandemic. Both ACE1 inhibitors and beta-adrenergic blockers reduce plasma concentrations of angiotensin II, the ACE2 substrate, for ACE1 inhibitors by reducing cleavage of angiotensin I to angiotensin II, and with beta-blockers by reducing release of renin from the kidneys. This might suggest they are potentially suitable replacements and preferred, because they potentially reduce ACE2 expression. Calcium channel blockers, another antihypertensive class mainstay, are neutral concerning angiotensin II availability, and potentially suitable. Diuretics and mineralocorticoid antagonists increase angiotensin II production, because of body sodium losses, which in the context of a COVID-19 pandemic might be adverse; sodium loading does reduce ACE2 expression. But in truth, inferences of ACE2 expression changes during antihypertensive dosing from known changes in angiotensin availability may possibly not be valid. The crucial point is that angiotensin receptor blocker drugs increase ACE2 expression remarkably, which is a significant demerit, emphasized by the fact that one favoured path of vaccine development is immunological antagonism of the ACE2 binding site for the SARS-CoV-2 virus spike protein. We have presented the hypothesis that prescribing of angiotensin receptor-blocking drugs during the COVID-19 pandemic might possibly be harmful, and suggested that other antihypertensive drug classes are preferred. We hope that the clinical data base from the pandemic so far could provide sufficient detail on hypertension diagnosis and antihypertensive drug prescribing to test our hypothesis. If the hypothesis was confirmed, how might this be applied clinically? One application would be in those SARS-CoV-2-infected patients who have a blood pressure rise during their acute illness, which has been noted. Any current dosing of ARB drugs should not be escalated, or new ARB therapy initiated. Perhaps ARBs currently prescribed should be entirely replaced in the acute illness by other antihypertensives as needed. The caveat here is that the rate at which excess ACE2 protein would disappear from cell membranes after discontinuation of ARBs is not known. More contentious, perhaps, would be the advice to replace ARBs with other antihypertensive agents as the pandemic approaches and intensifies. Although this is an option which should be considered, our recommendation at present is to not discontinue angiotensin receptor blockers prior to confirmation of the hypothesis. Any resulting destabilizing of blood pressure control in hypertension, which might possibly occur with treatment changes, would carry risks which are not just hypothetical. Simply discontinuing antihypertensives is strongly discouraged and is not an option. ACKNOWLEDGEMENTS Supported in part by the Victorian Government's Operational Infrastructure Support Program. Conflicts of interest There are no conflicts of interest.

In quadrupeds, the arterial baroreflex has dominance in the reflex homeostatic responses, which protect against haemorrhage. In humans, it is the low pressure cardiopulmonary reflex, which protects against the analogous cardiovascular challenge of gravity-dependent venous pooling with standing. To preserve orthostatic cardiovascular homeostasis with the emergence of bipedalism in humans the low pressure reflex, a minor, subsidiary reflex in quadripeds, was co-opted. Mirroring the imperfect skeletal evolution to bipedalism, this cardiovascular development has been problematic, with dysregulation manifesting as disabling orthostatic intolerance syndromes and, paradoxically, an orthostatic hypertensive response that appears to play a role in the development of essential hypertension in some people. Improved understanding of these evolutionary faults provides new options for postural and pharmacological treatments.

OBJECTIVE:To examine preventive health attendance and recording of type 2 diabetes and cardiovascular disease risk factors and their management in young Aboriginal peoples and Torres Strait Islanders (Indigenous Australians) at primary health care centres (PHCs). METHODS:This descriptive cross-sectional study audited medical records of 1,986 Indigenous people aged 15-34 years attending 93 Australian PHCs. Measurements included blood pressure (BP), blood glucose level (BGL), smoking status, body mass index (BMI) and lipid profile. RESULTS:Last attendance was most commonly for acute care (46%); 12% attended for preventive assessment. BP was recorded in 85% (1,686/1,986), BGL 63% (1,244/1,986), smoking status 52% (1,033/1,986), BMI 37% (743/1,986) and lipids 31% (625/1,986). Of those with a recorded assessment, elevated BGL (39%, 479/1,244), smoking (63%, 649/1,033), overweight/obesity (51%, 381/743) and dyslipidaemia (73%, 458/625) were common. Follow-up of abnormal results was documented for elevated BP 28% (34/120), elevated BGL 17% (79/479), smoking 65% (421/649), overweight/obesity 11% (40/381) and abnormal lipids 16% (75/458). CONCLUSIONS:These findings highlight the importance of raising awareness and assessment of chronic disease risk factors in young Indigenous people and implementing preventive health care strategies. IMPLICATIONS:Strengthening the capacity of PHCs to provide preventive health care may contribute to reducing the chronic disease burden experienced by young Indigenous people.

OBJECTIVE:Hypertension and other chronic disease risks are common among Aboriginal and Torres Strait Islander adults but there is little evidence regarding the epidemiology of these risk factors during adolescence. This study examines the prevalence of pre-hypertension, hypertension and other cardiovascular risk factors in Aboriginal and Torres Strait Islander people aged 15-24 years living in remote Indigenous communities in north Queensland. In so doing, it aims to better inform the approach to cardiovascular disease in this population. METHODS:This is a descriptive study that retrospectively examines health service data from a program of community screening, the Young Persons Check (YPC). Participants were 1,883 Aboriginal and Torres Strait Islander people aged 15-24 years who attended for a YPC in 11 remote communities in north Queensland between March 2009 and April 2011. RESULTS:Overall, the prevalence of pre-hypertension was 34.0%; stage I hypertension was 17.7% and stage II hypertension was 3.3%. The prevalence of elevated waist circumference was 47.6%, overweight or obesity 45.9%, elevated triglycerides 18.3%, decreased HDL 54.8% and proteinuria 24.3%. The prevalence of hypertension (stage I or II) among Torres Strait Islander males was 34.1%, Aboriginal males 26.9%, Torres Strait Islander females 12.6% and Aboriginal females 13.0%. Hypertension was associated with sex (males) (OR= 4.37, p<0.000), overweight (OR=2.46, p<0.000), obesity (OR=4.59, p<0.000) and elevated triglycerides (OR=2.38, p<0.000). CONCLUSION:Pre-hypertension, hypertension and other cardiovascular risk in this population is highly prevalent. Hypertension was particularly prevalent among male participants. The results reiterate the importance of early life experience in cardiovascular disease prevention.

Background: Health disparities between remote and urban living Australians have commonly been attributed to the relatively high proportion of the remote population that are Indigenous (1). Methods: This study retrospectively assessed service delivery data from people aged 15–24 years attending for a Young Person Check (YPC) in 7 remote communities in far north Queensland between March 2009 and April 2011. Data relating to the prevalence of hypertension, obesity, increased waist circumference, non-fasting blood sugar levels, non-fasting lipid profiles and proteinuria were analysed. Results: Among non-Indigenous YPC participants (n = 121) the prevalence of pre-hypertension was 36.7%, stage I hypertension was 15.6% and stage II hypertension was 0%. The prevalence of overweight or obesity was 46.7%, increased waist circumference was 33.1%, increased triglycerides was 14.3%, reduced HDL was 25.8%, proteinuria was 14.9%. The prevalence of hypertension (p value 0.218), probable diabetes (p value 0.395), overweight or obesity (p value 0.455) and elevated triglycerides (p value 0.273) did not differ between non-Indigenous and Indigenous participants. A lower proportion of non-indigenous participants had an elevated waist circumference (p value 0.002), reduced HDL (p value 0.000) and proteinuria (p value 0.018) than Indigenous participants. Conclusion: These remote living non-Indigenous young adults are experiencing a heavy burden of chronic disease risk. The alignment of much of this risk with that experienced by Indigenous participants highlights the importance of addressing social determinants of health in remote communities. It also supports the need to clearly identify and respond to the particular needs of remote living non-Indigenous youth. References Australian Institute of Health and Welfare 2004. Australia's health 2004. Canberra: AIHW.

Background: The burden of chronic disease in Aboriginal and Torres Strait Islander populations is well documented (1, 2, 3). This study retrospectively examines the prevalence of hypertension and other chronic disease risk factors in a sample of 1883 Aboriginal and Torres Strait Islander people aged 15-24 years that attended for a Young Person Check in 15 remote communities in far north Queensland between March 2009 and April 2011. Methods: Data relating to the prevalence of pre-hypertension, stage I hypertension, stage II hypertension, obesity, increased waist circumference, non-fasting blood sugar levels, non-fasting lipid profiles, proteinuria and albuminuria were analysed. Results: Overall the prevalence of pre-hypertension was 34.0%, stage I hypertension was 17.7% and stage II hypertension was 3.3%. The prevalence of elevated waist circumference was 47.6%, overweight or obesity 45.9%, elevated triglycerides 18.3%, decreased HDL 54.8% and proteinuria 24.3%. The prevalence of hypertension (stage I or II) among Torres Strait Islander males was 34.1%, Aboriginal males 26.9%, Aboriginal females 13.0% and Torres Strait Islander females 12.6%. The difference in hypertension prevalence between the genders was statistically significant.(p = 0.000 for both Aboriginal and Torres Strait Islanders) Conclusion: The study indicates that many remote living Indigenous youth are already on the trajectory towards chronic disease. Consequently, primary preventive activity directed at addressing the causes of chronic disease including overweight and obesity should be directed at children, their families and the environment in which the population lives. Screening for hypertension and other risk factors should commence by adolescence. ReferencesAustralian Bureau of Statistics and Australian Institute of Health and Welfare), The Health and Welfare of Australia's Aboriginal and Torres Strait Islander Peoples. Canberra, 2010Wang Z, Knight S, Wilson A, Rowley K G, Best J D, McDermott R, Leonard D, Shaw JE and O’Dea K. Blood pressure and hypertension for Australian Aboriginal and Torres Strait Islander people. European Journal of Cardiovascular Prevention and Rehabilitation 2006;13:438-443Miller G, McDermott R, McCulloch B, Leonard D, Arabena K, Muller R. The Well Person's Health Check: a population screening program in Indigenous communities in north Queensland. Australian Health Review 2002;25(6):136-147.

BACKGROUND:Pelvic instability is a term describing a group of conditions causing pelvic girdle pain in pregnancy. Although a common problem in pregnancy, it is easily overlooked and sometimes dismissed as 'normal' by primary care professionals.OBJECTIVE:This article outlines the clinical features, diagnosis and management of pelvic instability in pregnancy.DISCUSSION:General practitioners are in an ideal position to diagnose pelvic instability, implement treatment, and refer for further care to a physiotherapist with an interest in women's health. Use of a supportive belt or taping, appropriate analgesia, core stability and pelvic floor exercises, and avoiding heavy lifting and activities that exacerbate the pain are the mainstays of treatment.

BACKGROUND:Dengue virus infection is spread by the mosquito vector Aedes aegypti and causes significant morbidity and mortality worldwide. In Australia, it is an important cause of fever in the returned traveller and recent outbreaks have occurred in northern Queensland. A comprehensive understanding of the clinical and public health ramifications of dengue infection is essential for general practitioners.OBJECTIVE:The aim of this article is to review the pathophysiology, clinical manifestations, complications, laboratory investigations and public health consequences of dengue infection.DISCUSSION:Dengue should be considered as a differential diagnosis of fever in a returned traveller, including in patients who have travelled to northern Queensland within 3 months of an outbreak. Clinical manifestations vary from asymptomatic infection to serious disease. Typical symptoms last 7 days and may include: fever, headache, myalgia, fatigue, abnormal taste sensation, arthralgia, maculopapular rash and anorexia. Around 1% of patients will get the more severe form of the illness, dengue haemorrhagic fever. Recommended diagnostic tests depend on the time since the onset of symptoms. Management involves symptomatic treatment and monitoring for complications. Dengue haemorrhagic fever requires hospitalisation. Prompt notification to public health authorities and advice to patients about prevention of spread are a key role of the GP.

BACKGROUND:The Australian STI Prevention Framework identifies sex workers as a priority group. The Hunter New England Sexual Health Unit, based at the Royal Newcastle Hospital (New South Wales) provides free sexual health care to sex industry workers.OBJECTIVE:To assess current service delivery and barriers to accessing sexual health care by registered brothel based sex industry workers in the Hunter New England area.METHOD:An on site survey of 36 sex industry workers was conducted.RESULTS:Seventy-four percent of participants sought sexual health advice from a general practitioner compared to 37% from the sexual health unit. Seventy-seven percent of participants reported having their sexual health screening carried out according to guidelines. The most frequently stated reason for not using the sexual health unit was the inconvenience of clinic opening times.DISCUSSION:This study highlights the important role that GPs play in providing sexual health care to sex industry workers. It provides the impetus for future research, education and strategies to improve health service delivery to this important group of patients.

BACKGROUND:Participatory action research engenders change not just through research outcomes but through the research process itself. Collaboration between researchers and those being researched is intrinsic to the model. OBJECTIVE:This article discusses the 'Sadness and Heart Disease' research project undertaken by an Aboriginal community controlled health service in Darwin (Northern Territory) in 2005 and 2006 using a participatory action framework. DISCUSSION:A systematic approach, flexibility and a willingness to engage are necessary for researchers to successfully undertake a project using the participatory action framework. The benefits of participatory action research extend to both the community and the researchers.

OBJECTIVES:To assess the reliability and validity of a depression screening tool--the PHQ-9Pfizer Inc. modified for use with Aboriginal and Torres Strait Islander people. We also sought to determine the prevalence of depression in a sample of Indigenous people with ischaemic heart disease (IHD). METHODS:The modified PHQ-9 was administered to a sample of Indigenous people with IHD by an Aboriginal Health Worker (AHW). Tool results were then compared with the results of a psychiatric diagnostic interview conducted by a medical practitioner. Thirty four IHD patients attending an Aboriginal Community Controlled Health Service (ACCHS) in Darwin in 2006 and 2007 participated in the study. The modified PHQ-9's sensitivity, specificity, positive and negative predictive value were calculated for major and minor depression. Chronbach's alpha of the screening test was calculated to measure internal consistency. The prevalence of depression in the study group was also determined. RESULTS:The prevalence of major depression in the sample was 15.4% (95% CI 7.2%-29.7%). When assessing for major depression the modified PHQ-9 was 80% sensitive (95% CI 66.4-93.6%) and 71.4% (95% CI 56.0-86.8%) specific. A 'mini' version of the modified PHQ-9 demonstrated 100% sensitivity (95% CI 100%-100%) and 12.5% specificity (95% CI 7.0% -25.7%) Chronbach's alpha was 0.8. CONCLUSION:The modified PHQ-9 and the mini-tool, showed promise in this setting. Further investigation with a larger number of Aboriginal and Torres Strait Islander participants is warranted. IMPLICATIONS:This study has implications both for the Medicare funded Aboriginal Adult Health Checks and for program planning for Aboriginal IHD patients.

Polycystic ovary syndrome (PCOS) is a common endocrine disorder affecting 5-10% of women. It is characterised by androgenisation and anovulation, with sufferers being at increased risk of metabolic problems such as noninsulin dependent diabetes mellitus and dyslipidaemia. An increased risk of cardiovascular disease is speculated. Clinically, sufferers may experience acne, obesity, hirsutism and/or male pattern baldness.

OBJECTIVE:To assess the acceptability and face validity of a psychological assessment instrument, the Patient Health Questionnaire 9 (PHQ-9), as a depression screening tool for use with Aboriginal and Torres Strait Islander patients. METHODS:Four focus groups were held in an urban, Aboriginal community-controlled health service. Participants' attitudes to screening for depression and the specific components of PHQ-9 were explored. RESULTS:Process-oriented and PHQ-9-specific themes were raised. They included the role of family in the screening process, the need for a trusting relationship between the tool administrator and patient, the risk of confounding by social disadvantage or physical co-morbidities, the absence of a question assessing the presence of anger as a symptom of depression, and the importance of culturally appropriate language within the tool. CONCLUSION:Modification of the screening process and wording of the PHQ-9 in response to these concerns should render it acceptable for use with Aboriginal and Torres Strait Islander patients in this setting. IMPLICATIONS:These results may apply to the use of other psychological screening tools in the Aboriginal and Torres Strait Islander population. This is particularly relevant given the policy emphasis on screening in Indigenous health.

Australian guidelines for sexual history taking and sexually transmissible infection (STI) screening of HIV-positive patients do not exist. An audit was conducted to assess current practices of sexual history taking and STI testing of HIV-positive patients attending Hunter New England Sexual Health Unit.

The advent of new investigations for the detection of invasive meningococcal disease may lead to the diagnosis of milder forms of the infection which would previously have remained undiagnosed. In the context of mild disease there may be difficulty interpreting current guidelines and subsequently formulating an appropriate management and public health plan. This case study demonstrates the issues that may arise when positive serology results become available for a person with either partially, or un-treated mild invasive meningococcaemia. (non- author abstract)