Professor Jennifer Martin

Chair of Clinical Pharmacology

School of Medicine and Public Health

Career Summary


Professor Martin is a dual trained clinical pharmacologist and practising general physician. She has studied politics and health economics at Oxford University as a Rhodes Scholar and has used this experience to serve on the Pharmaceutical Benefits Advisory Committee, the Economic Subcommittee of the PBAC and other Government and Statewide committees examining appropriate allocation, regulation, safety and efficacy in pharmaceuticals. She is a Member of the Australian Institute of Company Directors (Diploma).

Her PhD (Monash) examined innate immunity in Type 2 diabetes and subsequent postdoctoral work at the Walter and Eliza Hall focussed on the function of macrophages with high fat diet. Her recent research is in the area of clinical development of both novel and old drugs for a variety of diseases and has developed a collaboration with Leiden University using clinical pharmacological methods generally to improve dosing, with EKUT (Germany) in the combined role of therapeutic drug monitoring (TDM) and pharmacogenetics to individualise choice and dose of chemotherapy, and with the National Institutes of Health in identifying and managing synthetic drugs of abuse.

Her current PhD students are researching cannabinoid therapies, targeted cancer therapies, dosing in neonates and therapeutic drug monitoring in clinical care including with antimicrobial therapies. Professor Martin is passionate about teaching in the area of clinical pharmacology and been involved in curriculum development for medical students (Otago, Monash, Queensland and Melbourne Universities) was the recent teaching and learning representative on the STC in clinical pharmacology for the College of Physicians (RACP). She is currently a member of the RACP Policy and Advocacy Committee, the Council of the Australasian Society for Clinical and Experimental Pharmacology and Therapeutics, and a member of the Pharmacology and Therapeutics Advisory Committee of PHARMAC, the sole purchaser for pharmaceuticals in New Zealand.

Research Expertise
Professor Jennifer Martin is Chair of Clinical Pharmacology in the School of Medicine and Public Health at the University of Newcastle and a practicing general physician at the Calvary Mater Hospital Newcastle.


  • PhD, Monash University
  • Bachelor of Medicine & Surgery, University of Otago - New Zealand
  • Master of Arts, University of Oxford - UK


  • Clinical pharmacology
  • Personalized medicine
  • Pharmaceutical pricing and regulation
  • Targeted therapies

Fields of Research

110399Clinical Sciences not elsewhere classified20
111204Cancer Therapy (excl. Chemotherapy and Radiation Therapy)30
111502Clinical Pharmacology and Therapeutics50

Professional Experience

UON Appointment

DatesTitleOrganisation / Department
17/10/2014 - Chair of Clinical PharmacologyUniversity of Newcastle
School of Medicine and Public Health

Academic appointment

DatesTitleOrganisation / Department
1/01/2013 - Membership National Prescribing Service Executive – RADAR
1/01/2013 - Membership Diamantina Health Partners Symposium Organising Committee
1/01/2013 - Membership IATDMCT Oncology Committee
1/01/2012 - MembershipDiamantina Health Partners Evidence and Innovation Theme
1/01/2012 - Membership Diamantina Health Partners Neuroscience and Recovery Centre Steering Committee
1/01/2011 - Editorial Board Journal Clinical Toxicology
1/01/2011 - Membership IATDMCT Standard Laboratory Practices (SLP) committee
1/01/2011 - Membership Queensland Health Improving Presribing Steering Committee
1/01/2010 - Editorial Board British Journal of Clinical Pharmacology
1/01/2010 - Editorial Board Therapeutic Advances in Drug Safety
1/01/2010 - Membership Association of Scientific and Clinical Pharmacologists and Toxicologists
1/01/2010 - MembershipAustralian Society of Clinical and Experimental Pharmacologists and Toxicologists
1/01/2010 - Membership Clinical Advisory Group “Closing the Divide in Indigenous Cancer” Queensland Institute Medical Research
1/01/2010 - Membership Editorial Advisory Group National Prescribing Service
1/01/2010 - Membership PAH Clinical Council
1/01/2010 - Membership UQ Discipline of Medicine Research Symposium Organising Committee and Sessional Chair
1/01/2010 - MembershipUniversity of South Australia Sansom Institute Research Advisory Board
1/01/2009 - Membership Medical Journal of Australia (MJA) Insight; Australian Doctor
1/01/2008 - MembershipQH Medicines Advisory Committee
1/01/2008 - Membership Queensland Health Medicines Advisory Committee
1/01/2007 - Editorial Board Australian Prescriber
1/01/2007 - Editorial Board Internal Medicine Journal
1/01/2007 - Membership Pharmacogenetics; Education ASCEPT (SIG)
1/01/2007 - Membership Medical Observer
1/01/2006 - Editorial Board Australian Medicine Handbook
1/01/2005 - 31/12/2009Membership Therapeutic Guidelines Working Group



2014Finalist Royal Australasian College of Physicians Teaching Award
Royal Australiasian College of Physicians (RACP)
2010Finalist Clinical Educator of the Year
Postgraduate Medical Council Queensland (Australia)
2010Nominee Teaching Award for Junior Medical Staff
PA (Princess Alexandra Hospital) Health Symposium


1999"Best Registrar" teaching award for 5th year medical students
Christchurch School of Medicine, Otago University (New Zealand)
1998"Best Registrar" teaching award for 4th year medical students
Christchurch School of Medicine, Otago University (New Zealand)

Research Award

2014University of Queensland Teaching Award
RBWH Clinical School, Faculty of Health Sciences, University of Queensland (Australia)


For publications that are currently unpublished or in-press, details are shown in italics.

Chapter (14 outputs)

2012Martin JH, Somogyi A, 'Pharmacogenomics and Warfarin Therapy', Therapeutic Drug Monitoring, Academic Press, London 161-174 (2012)
2007Martin JH, 'Contraception', Therapeutic Guidelines 2007, Therapeutic Guidelines 2007, . . (2007)
2007Martin JH, Krum H, 'Statin therapy in the prevention and treatment of heart failure', The Year In Heart Failure, Clinical Publishing, Atlas Medical Publishing, UK . (2007)
2007Martin JH, 'Getting to know your drugs', Therapeutic Guidelines, Therapeutic Guidelines 2007 Endocrinology Group, . 161-174 (2007)
2007Martin JH, Krum H, Gilbert R, 'Interactions between antihypertensive drugs and other medications', Comprehensive hypertension, Elsevier, New York (2007)
2006Martin JH, 'Cardiovascular Drugs', Australian Medicines Handbook (7th Ed), Australian Medicines Handbook, Melbourne . (2006)
2003Martin JH, Sim M, Hulse G, 'Opioids', Alcohol and Drug Problems- A Case Studies Workbook, Oxford University Press, South Melbourne 1-34 (2003)
2003Martin JH, Liew D, Johnson S, 'Benzodiazepines', Alcohol and Drug Problems - A Case Studies Workbook, Oxford University Press, South Melbourne 132-157 (2003)
2003Martin JH, Johnson S, Liew D, 'Cannabis, Hallucucinogens and CNS Stimulants', Alcohol and Drug Problems - A Case Studies Workbook, Oxford University Press, South Melbourne 61-97 (2003)
2002Martin JH, Krum H, Haas S, Gilbert R, 'Metabolic co-morbid conditions in heart failure: Diabetes and hypercholesterolemia', Heart Failure Annual, Heart Failure Annual, London 35-58 (2002)
2002Martin JH, Cape G, Hulse G, Robinson G, McLean S, Saunders J, Young R, 'Sedative-Hypnotics', Management of alcohol and drug problems, Oxford University Press, Adelaide 212-227 (2002)
2002Martin JH, Todd F, McLean S, Krum H, Copeland J, 'Cannabis', Management of alcohol and drug problems, Oxford University Press, Adelaide 141-157 (2002)
2002Martin JH, White J, Krum H, McLean S, Young R, Saunders J, 'Hallucinogens', Management of alcohol and drug problems, Oxford University Press, Adelaide 229-238 (2002)
2002Martin JH, Young R, Saunders J, Hulse G, McLean S, Robinson G, 'Opiods', Management of alcohol and drug problems, Oxford University Press, Adelaide 79-99 (2002)
Show 11 more chapters

Journal article (120 outputs)

2015Hubbard RE, Peel NM, Scott IA, Martin JH, Smith A, Pillans PI, et al., 'Polypharmacy among inpatients aged 70 years or older in Australia.', Med J Aust, 202 373-377 (2015)
Author URL
2015Lim AE, Tate JR, Clarke D, Norris RL, Morris RG, Martin JH, 'Clinical Consequences of a Miscalibrated Digoxin Immunoassay', THERAPEUTIC DRUG MONITORING, 37 104-109 (2015)
Author URL
2015Lindsay J, Dooley M, Martin J, Fay M, Kearney A, Khatun M, Barras M, 'The development and evaluation of an oncological palliative care deprescribing guideline: the 'OncPal deprescribing guideline'', SUPPORTIVE CARE IN CANCER, 23 71-78 (2015)
DOI10.1007/s00520-014-2322-0Author URL
2015Liu X, Vitetta L, Kostner K, Crompton D, Williams G, Brown WJ, et al., 'The effects of tai chi in centrally obese adults with depression symptoms', Evidence-based Complementary and Alternative Medicine, 2015 (2015)

This study examined the effects of Tai Chi, a low-impact mind-body movement therapy, on severity of depression, anxiety, and stress symptoms in centrally obese people with elevated depression symptoms. In total, 213 participants were randomized to a 24-week Tai Chi intervention program or a wait-list control group. Assessments were conducted at baseline and 12 and 24 weeks. Outcomes were severity of depression, anxiety, and stress symptoms, leg strength, central obesity, and other measures of metabolic symptom. There were statistically significant between-group differences in favor of the Tai Chi group in depression (mean difference = -5.6 units, P < 0.001), anxiety (-2.3 units, P < 0.01), and stress (-3.6 units, P < 0.001) symptom scores and leg strength (1.1 units, P < 0.001) at 12 weeks. These changes were further improved or maintained in the Tai Chi group relative to the control group during the second 12 weeks of follow-up. Tai Chi appears to be beneficial for reducing severity of depression, anxiety, and stress and leg strength in centrally obese people with depression symptoms. More studies with longer follow-up are needed to confirm the findings. This trial is registered with ACTRN12613000010796.

2015Martin JH, Ferro A, 'From an evolutionary perspective, all 'new' antimicrobial targets are old: time to think outside the box.', Br J Clin Pharmacol, 79 165-167 (2015)
DOI10.1111/bcp.12385Author URL
2015Hosein AN, Lim YC, Day B, Stringer B, Rose S, Head R, et al., 'The effect of valproic acid in combination with irradiation and temozolomide on primary human glioblastoma cells.', J Neurooncol, 122 263-271 (2015)
DOI10.1007/s11060-014-1713-xAuthor URL
2015Fay M, Head R, Martin J, 'Where is the radiobiology and pharmacology research to improve outcomes in glioblastoma?', Journal of Neuro-Oncology, (2015)

Personalized medicine has been helpful for drug development in diseases with single and relatively stable gene mutations. The benefit for complex solid tumours with heterogeneous and changing genetic profiles is less clear. Whether it is efficient to continue diverting resources from combined biological and pharmacological approaches to trial new and existing genetic ¿targeted therapies¿ for brain tumours is unknown but of developing concern in resource constrained environments.

2015Valery PC, Powell E, Moses N, Volk ML, McPhail SM, Clark PJ, Martin J, 'Systematic review: unmet supportive care needs in people diagnosed with chronic liver disease', BMJ OPEN, 5 (2015)
DOI10.1136/bmjopen-2014-007451Author URL
2015Diaz A, Moore SP, Martin JH, Green AC, Garvey G, Valery PC, 'Factors associated with cancer-specific and overall survival among Indigenous and non-Indigenous gynecologic cancer patients in Queensland, Australia: a matched cohort study.', Int J Gynecol Cancer, 25 542-547 (2015)
DOI10.1097/IGC.0000000000000375Author URL
2015Scott IA, Hilmer SN, Reeve E, Potter K, Le Couteur D, Rigby D, et al., 'Reducing inappropriate polypharmacy: the process of deprescribing.', JAMA Intern Med, 175 827-834 (2015)
DOI10.1001/jamainternmed.2015.0324Author URL
CitationsScopus - 3
2014Williams MM, Taylor PJ, Page CB, Martin JH, 'Clinical research in synthetic cannabinoids - do we need a national approach?', Med J Aust, 201 317-319 (2014) [C3]
Author URL
CitationsScopus - 1
2014Morais C, Small D, Vesey D, Martin JH, Johnson D, Gobe G, 'Fibronectin and transforming growth factor beta contribute to erythropoietin resistance and maladaptive cardiac hypertrophy', Biochemical and Biophysical Research Communications, 444 332-337 (2014)
2014Theile DE, Scott IA, Martin JH, Gavrilidis A, 'Enabling the success of academic health science centres in Australia: where is the leadership?', The Medical journal of Australia, 201 636-638 (2014) [C3]
CitationsScopus - 1
2014Sullivan CM, Staib A, Flores J, Aggarwal L, Scanlon A, Martin JH, Scott IA, 'Aiming to be NEAT: Safely improving and sustaining access to emergency care in a tertiary referral hospital', Australian Health Review, 38 564-574 (2014)
2014Arpon DR, Gandhi MK, Martin JH, 'A new frontier in haematology - Combining pharmacokinetic with pharmacodynamic factors to improve choice and dose of drug', British Journal of Clinical Pharmacology, 78 274-281 (2014)

The issue of tailored dosing adjusted according to a range of patient-specific factors other than bodyweight or body surface area is of large and increasing clinical and financial concern. Even if it is known that dosing alterations are likely to be required for parameters such as body composition, gender and pharmacogenetics, the amount of dosing change is unknown. Thus, pharmacokinetically guided dosing is making a resurgence, particularly in areas of medicine where there are cost constraints or safety issues, such as in haematology medications. However, the evidence to support the behaviour is minimal, particularly when long-term outcomes are considered. In haematology, there are particular issues around efficacy, toxicity and overall cost. Newer targeted agents, such as the monoclonal antibody rituximab and the tyrosine kinase inhibitor imatinib, whilst clearly being highly effective, are dosed on a milligram per square metre (rituximab) or fixed dose basis (imatinib), regardless of body composition, tumour aspects or comorbidity. This review questions this practice and raises important clinical issues; specifically, the clinical potential for combined pharmacokinetically and pharmacodynamically guided dosing of new targeted agents in haematological malignancies. This pharmacokinetically and pharmacodynamically guided dosing is an emerging area of clinical pharmacology, driven predominantly by toxicity, efficacy and cost issues, but also because reasonable outcomes are being noted with more appropriately dosed older medications adjusted for patient-specific factors. Clinical trials to investigate the optimization of rituximab dose scheduling are required. © 2014 The British Pharmacological Society.

CitationsScopus - 1
2014Lindsay J, Dooley M, Martin J, Fay M, Kearney A, Barras M, 'Reducing potentially inappropriate medications in palliative cancer patients: evidence to support deprescribing approaches', SUPPORTIVE CARE IN CANCER, 22 1113-1119 (2014)
DOI10.1007/s00520-013-2098-7Author URL
CitationsWeb of Science - 3
2014Leung J, McKenzie S, Martin JH, Dobson A, McLaughlin D, 'Longitudinal patterns of breast cancer screening: Mammography, clinical, and breast self-examinations in a rural and urban setting', Women's Health Issues, 24 e139-e146 (2014)
2014Carroll JP, Protani MM, Linda N, Cheng ME, Fay M, Saleem M, et al., 'Toxicity and tolerability of adjuvant breast cancer chemotherapy in obese women', MEDICAL ONCOLOGY, 31 (2014)
DOI10.1007/s12032-014-0881-zAuthor URL
CitationsScopus - 2Web of Science - 2
2014Fay MF, Martin JH, Rose S, 'New imaging techniques for more effective treatment in glioblastoma', Internal Medicine Journal, 44 5-6 (2014) [C3]
2014Martin JH, Coombes I, 'Mortality from common drug interactions systems, knowledge and clinical reasoning to optimise prescribing', Internal Medicine Journal, 44 621-624 (2014) [C3]
2014Fagan KJ, Irvine KM, McWhinney BC, Fletcher LM, Horsfall LU, Johnson L, et al., 'Diagnostic sensitivity of carbohydrate deficient transferrin in heavy drinkers', BMC GASTROENTEROLOGY, 14 (2014)
DOI10.1186/1471-230X-14-97Author URL
CitationsWeb of Science - 1
2014Moore SP, Green AC, Bray F, Garvey G, Coory M, Martin J, Valery PC, 'Survival disparities in Australia: an analysis of patterns of care and comorbidities among indigenous and non-indigenous cancer patients', BMC CANCER, 14 (2014)
DOI10.1186/1471-2407-14-517Author URL
CitationsWeb of Science - 2
2014Chachay VS, Macdonald GA, Martin JH, Whitehead JP, O'Moore-Sullivan TM, Lee P, et al., 'Resveratrol Does Not Benefit Patients With Nonalcoholic Fatty Liver Disease', CLINICAL GASTROENTEROLOGY AND HEPATOLOGY, 12 2092-U383 (2014)
DOI10.1016/j.cgh.2014.02.024Author URL
CitationsScopus - 4Web of Science - 7
2014Chachay VS, Macdonald GA, Martin JH, Whitehead JP, O'Moore-Sullivan TM, Lee P, et al., 'Resveratrol Does Not Benefit Patients With Nonalcoholic Fatty Liver Disease', Clinical Gastroenterology and Hepatology, 12 2092-2103 (2014) [C1]

Background & Aims: Nonalcoholic fatty liver disease (NAFLD), characterized by accumulation of hepatic triglycerides (steatosis), is associated with abdominal obesity, insulin resistance, and inflammation. Although weight loss via calorie restriction reduces features of NAFLD, there is no pharmacologic therapy. Resveratrol is a polyphenol that prevents high-energy diet-induced steatosis and insulin resistance in animals by up-regulating pathways that regulate energy metabolism. We performed a placebo-controlled trial to assess the effects of resveratrol in patients with NAFLD. Methods: Overweight or obese men diagnosed with NAFLD were recruited from hepatology outpatient clinics in Brisbane, Australia from 2011 through 2012. They were randomly assigned to groups given 3000 mg resveratrol (n= 10) or placebo (n= 10) daily for 8 weeks. Outcomes included insulin resistance (assessed by the euglycemic-hyperinsulinemic clamp), hepatic steatosis, and abdominal fat distribution (assessed by magnetic resonance spectroscopy and imaging). Plasma markers of inflammation, as well as metabolic, hepatic, and antioxidant function, were measured; transcription of target genes was measured in peripheral blood mononuclear cells. Resveratrol pharmacokinetics and safety were assessed. Results: Eight-week administration of resveratrol did not reduce insulin resistance, steatosis, or abdominal fat distribution when compared with baseline. No change was observed in plasma lipids or antioxidant activity. Levels of alanine and aspartate aminotransferases increased significantly among patients in the resveratrol group until week 6 when compared with the placebo group. Resveratrol did not significantly alter transcription of NQO1, PTP1B, IL6, or HO1 in peripheral blood mononuclear cells. Resveratrol was well-tolerated. Conclusions: Eight weeks administration of resveratrol did not significantly improve any features of NAFLD, compared with placebo, but it increased hepatic stress, based on observed increases in levels of liver enzymes. Further studies are needed to determine whether agents that are purported to mimic calorie restriction, such as resveratrol, are safe and effective for complications of obesity. Clinical trials registration no: ACTRN12612001135808.

CitationsScopus - 18
2014Jellis CL, Sacre JW, Wright J, Jenkins C, Haluska B, Jeffriess L, et al., 'Biomarker and imaging responses to spironolactone in subclinical diabetic cardiomyopathy.', European heart journal cardiovascular Imaging, 15 776-786 (2014) [C1]
2013Martin JH, Fagan K, Irvine K, McWhinney B, Fletcher L, Horsfall L, et al., 'BMI but not aetiology or stage of liver disease affects the diagnostic sensitivity of carbohydrate deficient transferrin', Alcoholism: Clinical and Experimental Research, 37 1771-1778 (2013)
2013Martin JH, Hubbard RE, Peel NM, Scott IA, Pillans PI, Gray LC, 'Polypharmacy among Older Inpatients in Australia', Australasian Journal on Ageing, 32 24 (2013)
2013Martin JH, 'Smoking and drug interactions', Australian Prescriber, 36 102-104 (2013)
2013Martin JH, Chachay V, Prins J, Whitehead J, O'Moore-Sullivan T, Lee P, et al., 'Investigating the clinical effect of resveratrol in non-alcoholic fatty liver disease: a randomised, double blind, placebo-controlled trial', Journal of Gastroenterology and Hepatology, 28 78-79 (2013)
2013Martin JH, Forbes M, Raj A, Lampe G, Powell E, '"Khat-associated hepatitis"', Medical Journal of Australia, 199 498-499 (2013)
2013Fagan KJ, Irvine KM, McWhinney BC, Fletcher LM, Horsfall LU, Johnson LA, et al., 'BMI But Not Stage or Etiology of Nonalcoholic Liver Disease Affects the Diagnostic Utility of Carbohydrate-Deficient Transferrin', ALCOHOLISM-CLINICAL AND EXPERIMENTAL RESEARCH, 37 1771-1778 (2013)
DOI10.1111/acer.12143Author URL
CitationsScopus - 2Web of Science - 2
2013Chachay VS, Martin JH, Prins JB, Whitehead JP, O'Moore-Sullivan TM, Lee P, et al., 'Investigating the clinical effect of resveratrol in non-alcoholic fatty liver disease: A randomised, double blind, placebo-controlled trial', JOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, 28 78-79 (2013) [E3]
Author URL
2013Phillips LK, Peake JM, Zhang X, Hickman IJ, Briskey DR, Huang BE, et al., 'Postprandial total and HMW adiponectin following a high-fat meal in lean, obese and diabetic men', European Journal of Clinical Nutrition, 67 377-384 (2013)

Background/Objectives: Recent work suggests that macronutrients are pro-inflammatory and promote oxidative stress. Reports of postprandial regulation of total adiponectin have been mixed, and there is limited information regarding postprandial changes in high molecular weight (HMW) adiponectin. The aim of this study was to assess the effect of a standardised high-fat meal on metabolic variables, adiponectin (total and HMW), and markers of inflammation and oxidative stress in: (i) lean, (ii) obese non-diabetic and (iii) men with type 2 diabetes mellitus (T2DM). Subjects/Methods: Male subjects: lean (n=10), obese (n=10) and T2DM (n=10) were studied for 6 h following both a high-fat meal and water control. Metabolic variables (glucose, insulin, triglycerides), inflammatory markers (interleukin-6 (IL6), tumour necrosis factor (TNF)a, high-sensitivity C-reactive protein (hsCRP), nuclear factor (NF)¿B expression in peripheral blood mononuclear cells (p65)), indicators of oxidative stress (oxidised low density lipoprotein (oxLDL), protein carbonyl) and adiponectin (total and HMW) were measured.Results:No significant changes in TNFa, p65, oxLDL or protein carbonyl concentrations were observed. Overall, postprandial IL6 decreased in subjects with T2DM but increased in lean subjects, whereas hsCRP decreased in the lean cohort and increased in obese subjects. There was no overall postprandial change in total or HMW adiponectin in any group. Total adiponectin concentrations changed over time following the water control, and the response was significantly different in lean subjects compared with subjects with T2DM (P=0.04).Conclusions:No consistent significant postprandial inflammation, oxidative stress or regulation of adiponectin was observed in this study. Findings from the water control suggest differential basal regulation of total adiponectin in T2DM compared with lean controls. © 2013 Macmillan Publishers Limited All rights reserved.

CitationsScopus - 6
2013Dimeski G, Silvester B, Ungerer J, Johnson L, Martin JH, 'Policy change to improve pathology turnaround time and reduce costs - Possible to do both?', Biochemia Medica, 23 296-302 (2013)

Background: Overcrowding and prolonged length of stay in emergency departments (ED) are increasing problems in hospitals. Rapid availability of all laboratory results has an impact on clinical decision-making, admissions or discharge decisions and resource utilisation. Increasing number of our urinary drugs of abuse (DOA) screens had a turnaround time (TAT) of up to 33 days after the discharge of the patient. Materials and methods: Following an audit and a consultation period with clinicians using the service, a policy change was implemented to reduce the use of gas chromatography mass spectroscopy (GCMS): all requests would have a standard immunoassay (IA) test panel undertaken unless specifically they requested GCMS (including medico-legal) analysis. Results: Almost all of the clinicians interviewed had no understanding of the DOA screening or the difference in the information generated between a confirmatory GCMS urine toxicology screen and IA DOA panel. It appeared none of the patients surveyed in the audit would have had a different clinical decision made if a GCMS had not been undertaken. Post change audit showed only 4.3% of drug requests for IA also received a confirmatory GCMS testing. The estimated saving post change implementation was $127,000 (AU $) in test costs alone over a two year period. The TAT of GCMS results was reduced to 3-4 days. Conclusion: A laboratory-led behavioural change in test requesting is possible and sustainable provided the reason is clinically sound and accompanied by consultation and availability of advice by phone when requested on test requesting or interpretation. © Croatian Society of Medical Biochemistry and Laboratory Medicine.

CitationsScopus - 1
2013Scott IA, Gray LC, Martin JH, Pillans PI, Mitchell CA, 'Deciding when to stop: Towards evidence-based deprescribing of drugs in older populations', Evidence-Based Medicine, 18 121-124 (2013) [C3]

Minimising the harm from inappropriate prescribing in older populations is a major urgent concern for modern healthcare systems. In everyday encounters between prescribers and patients, opportunities should be taken to identify patients at high risk of harm from polypharmacy and reappraise their need for specific drugs. Attempts to reconcile life expectancy, comorbidity burden, care goals and patient preferences with the benefits and harms of medications should be made in every patient at significant risk. Drugs identified by this process of reconciliation as conferring little or no benefit and/or excessive risk of harm should be candidates for discontinuation. Evidence supporting a structured approach to drug discontinuation (or deprescribing) is emerging, and while many barriers to deprescribing exist in routine practice, various enabling strategies can help overcome them.

CitationsScopus - 9
2012Martin JH, Valery PC, Moore SP, Coory M, Martin J, Garvey G, Green AC, 'Advanced stage at diagnosis and worse comorbidity explain overall survival disparities between Indigenous and non-Indigenous cancer patients in Queensland', Asia Pac J Clin Oncol, 8 212* (2012)
2012Martin JH, Moore SP, Diaz A, Green AC, Garvey G, Coory M, Valery PC, 'Indigenous women with gynaecological cancers have poorer survival than non-Indigenous women: Explained by stage, comorbidity and treatment uptake', Asia Pac J Clin Oncol, 8 321 (2012)
2012Martin JH, Moore S, Green A, Garvey G, Corry M, Valery P, 'Breast Cancer diagnosis and patterns of treatment: does being indigenous make a difference?', Asia-Pacific Journal of Clinical Oncology, 8 304 (2012)
2012Martin JH, Jellis C, Sacre J, Wright J, Jenkins C, Jeffriess L, et al., 'A Randomised Trial of Spironolactone use in Subclinical Diabetic Cardiomyopathy: Anti-Fibrotic Effects on Myocardial Structure and Function', Heart Lung and Circulation, 21 . (2012)
2012Martin JH, Yamashiro Y, Gazarian M, Kling S, Nakamura H, Matsui A, et al., 'Drug Development: The Use of Unlicensed/Off-label Medicines in Pedatrics', J Clin Gastroenterol Nurt, 55 506-510 (2012)
2012Martin JH, Barras M, Yui NA, Kirkpatrick C, Kubler P, Norris R, 'Gentamicin Monitoring Practices in Teaching Hospitals ¿ Time to Undertake the Necessary Randomised Controlled Trial', J Clinic Toxicol, 2 146 (2012)
2012Martin JH, Norris R, Barra M, 'Gentamicin Use ¿ More Clinical Outcome Evidence Needed', J Clinic Toxicol, 2 e110 (2012)
2012Scott IA, Gray LC, Martin JH, Mitchell CA, 'Minimizing inappropriate medications in older populations: A 10-step conceptual framework', American Journal of Medicine, 125 (2012)

The increasing burden of harm resulting from the use of multiple drugs in older patient populations represents a major health problem in developed countries. Approximately 1 in 4 older patients admitted to hospitals are prescribed at least 1 inappropriate medication, and up to 20% of all inpatient deaths are attributable to potentially preventable adverse drug reactions. To minimize this drug-related iatrogenesis, we propose a quality use of medicine framework that comprises 10 sequential steps: 1) ascertain all current medications; 2) identify patients at high risk of or experiencing adverse drug reactions; 3) estimate life expectancy in high-risk patients; 4) define overall care goals in the context of life expectancy; 5) define and confirm current indications for ongoing treatment; 6) determine the time until benefit for disease-modifying medications; 7) estimate the magnitude of benefit versus harm in relation to each medication; 8) review the relative utility of different drugs; 9) identify drugs that may be discontinued; and 10) implement and monitor a drug minimization plan with ongoing reappraisal of drug utility and patient adherence by a single nominated clinician. The framework aims to reduce drug use in older patients to the minimum number of essential drugs, and its utility is demonstrated in reference to a hypothetic case study. Further studies are warranted in validating this framework as a means for assisting clinicians to make more appropriate prescribing decisions in at-risk older patients. © 2012 Elsevier Inc.

CitationsScopus - 33
2012Martin JH, Coory MD, 'New medicines - urgent need to assess outcomes in special groups', Medical Journal of Australia, 196 433-434 (2012)
CitationsScopus - 3
2012Martin JH, Theile DE, Ho KKY, Frazer IH, 'Diamantina health partners: Integrating leadership in research, research translation, education and clinical care', Medical Journal of Australia, 196 237-239 (2012)
CitationsScopus - 3
2012Saleem M, Dimeski G, Kirkpatrick CM, Taylor PJ, Martin JH, 'Target Concentration Intervention in Oncology: Where Are We At?', THERAPEUTIC DRUG MONITORING, 34 257-265 (2012)
DOI10.1097/FTD.0b013e3182557342Author URL
CitationsScopus - 12Web of Science - 9
2012Carroll J, Protani M, Walpole E, Martin JH, 'Effect of obesity on toxicity in women treated with adjuvant chemotherapy for early-stage breast cancer: A systematic review', Breast Cancer Research and Treatment, 136 323-330 (2012)

The purpose of this study is to provide more definite evidence regarding the role of dose modification of chemotherapy in obese women with breast cancer by systematically reviewing current literature regarding chemotherapy- induced toxicity rates in obese and non-obese women with early-stage breast cancer. A systematic search of Pubmed and EMBASE was conducted to identify original studies investigating chemotherapy-induced toxicity in obese women receiving adjuvant chemotherapy treatment for breast cancer. Ten studies were identified. We noted low rates of adjustment for confounders such as prophylactic hematopoietic growth factor use and empirical dose reductions. Seven studies found reduced toxicity in obese compared to non-obese women. Of four studies, where dose capping was precluded or statistically adjusted for, three found reduced toxicity in obese women. These outcomes include less febrile neutropenia (body mass index (BMI)<23.6; odds ratio (OR) 4.4; 95 % confidence interval (CI) 1.65-12.01), fewer hospital admissions (BMI <35; OR 0.61, 95 % CI 0.38-0.97), and fewer neutropenic events (BMI<25; OR 0.49; 95 % CI 0.37-0.66). Only a single study reported higher rates of toxicity in obese women, but this study had significant methodological issues. As a conclusion, we observed that obese patients tolerate chemotherapy better than lean patients. However, this may be confounded by poorly specified dose capping practices and the use of hematopoietic growth factors. Further research should focus on improved documentation of body size, of dose, and of use of growth factors, and analysis of how these affect recurrence rates, toxicity, and survival. © Springer Science+Business Media, LLC. 2012.

CitationsScopus - 7
2012Roberts JA, Norris R, Paterson DL, Martin JH, 'Therapeutic drug monitoring of antimicrobials', BRITISH JOURNAL OF CLINICAL PHARMACOLOGY, 73 27-36 (2012)
DOI10.1111/j.1365-2125.2011.04080.xAuthor URL
CitationsScopus - 39Web of Science - 28
2012Martin JH, Saleem M, Looke D, 'Therapeutic drug monitoring to adjust dosing in morbid obesity - a new use for an old methodology', British Journal of Clinical Pharmacology, 73 685-690 (2012)

The phenomena of hunger and need at one end of the spectrum and obesity and plenty on the other is an anomaly of the 21

st century, likely to be due to a combination of distributive inequities in food, social justice, access to education and other socio-economic factors. Both are major problems worldwide, although obesity has more media coverage due to the exponentially increasing incidence and the huge social and economic burden this is placing on Western society. For example, prevalence rates of obesity are currently exceeding 30% of adults in the USA with direct morbidity and mortality complications, in addition to the additional obesity-related health problems and death. Obesity is also rising in children. Obese people are thus a sizable group, and as with those with altered renal or liver function, require specific consideration with respect to the appropriate dosing of medications. However guidelines for how to do this in obesity are not currently available, due to the paucity of literature and regulatory rules for new medications which usually only request the demonstration of average population effectiveness. We believe it is timely for regulatory agencies worldwide to mandate studies involving consideration of body size, particularly obesity, in approving new medications across the therapeutic spectrum. This will drive the pharmaceutical industry to consider these groups in studies and will encourage investigator-initiated research using therapeutic drug monitoring (TDM), target concentration therapy (TCI) and pharmacogenetic (PGx) studies to optimize drug dosing. © 2011 The Authors. British Journal of Clinical Pharmacology © 2011 The British Pharmacological Society.

CitationsScopus - 5
2012Scott IA, Gray LC, Martin JH, Mitchell CA, 'Effects of a drug minimization guide on prescribing intentions in elderly persons with polypharmacy.', Drugs & aging, 29 659-667 (2012)
2012Scott IA, Gray LC, Martin JH, Mitchell CA, 'Effects of a drug minimization guide on prescribing intentions in elderly persons with polypharmacy', Drugs and Aging, 29 659-667 (2012)

Background: While frameworks exist to assist clinicians in prescribing appropriately in older patients at risk of adverse drug reactions, their impact on prescribing is uncertain. Objective: The aim of the study was to determine the effects of a ten-step drug minimization guide on clinician prescribing intentions involving a hypothetical older patient receiving multiple drugs. Methods: A total of 61 hospital clinicians were presented with clinical information about a hypothetical case: an 81-year-old female with 12 chronic diseases, receiving 19 different medications. On a standardized, anonymous form, each participant indicated, as a pre-test, which drugs they felt strongly inclined to discontinue or continue, and which drugs they were uncertain about. The ten-step guide was then presented and applied to the case, and participants repeated the drug selection process. Results: Sixty evaluable forms were analysed from 19 consultant physicians, 17 medical registrars, 7 interns/residents and 17 pharmacists. Among the entire cohort, the mean (-SD) number of drugs selected for discontinuation increased from 6.0 (-2.7) pre-test to 9.6 (-3.2) post-test (p < 0.001), with the greatest increases seen among consultant physicians (6.6 [-2.3] to 11.5 [-2.9], p < 0.001) and clinical pharmacists (5.3 [-2.6] to 8.9 [-2.2], p < 0.001). The number of drugs associated with uncertainty decreased from 3.7 (-2.9) pretest to 1.8 (-2.3) post-test (p < 0.001) for the whole cohort, with the greatest decreases seen among consultant physicians (4.8 [-2.6] to 1.8 [-2.5], p < 0.001) and clinical pharmacists (4.5 [-3.3] to 1.9 [-2.0], p = 0.003). Conclusion: This self-report study involving a hypothetical case provides evidence that a drug minimization guide may reduce inappropriate prescribing and uncertainty around drug indications. © 2012 Springer International Publishing AG. All rights reserved.

CitationsScopus - 8
2012Martin JH, Coory M, Baade P, 'Challenges of an ageing and dispersed population for delivering cancer services in Australia: More than just doctors needed', Internal Medicine Journal, 42 349-351 (2012)
CitationsScopus - 2
2012Duley JA, Somogyi AA, Martin JH, 'The future of thiopurine pharmacogenomics', Pharmacogenomics, 13 1549-1552 (2012)
CitationsScopus - 3
2011Martin JH, Jellis CL, Stanton T, Leano R, Marwick TH, 'Usefulness of at rest and exercise hemodynamics to detect subclinical myocardial disease in type 2 diabetes mellitus', American Journal of Cardiology, 107 615-621 (2011)
2011Martin JH, Jacka C, Garvey G, Sabesan S, Ghandi M, Baxi S, et al., 'Closing the Divide in Indigenous cancer: Cancer brochures for Indigenous patients and their families', Asia Pacific Journal of Clinical Oncology, 7 147 (2011)
2011Martin JH, Jellis C, Wrigh J, Kennedy D, Sacre J, Jenkins C, et al., 'Association of Imaging Markers of Myocardial Fibrosis with Metabolic and Functional Disturbances in Early Diabetic Cardiomyopathy', Circulation: Cardiovascular Imaging, 4 693-702 (2011)
2011Martin JH, Scott I, Mitchell C, Gray L, 'Optimising drug use in elderly populations ¿ pilot study of a drug minimization guide', Internal Medicine Journal, 41 14 (2011)
2011Martin JH, Jellis C, Sacre JW, Haluska B, Jenkins C, Marwick TH, 'Myocardial Dysfunction and Metabolic Derangement in Type 2 Diabetes: Relationship with Procollagen Biomarkers of Myocardial Fibrosis', Journal American College of Cardiology, 57 860 (2011)
2011Martin JH, Garvey G, Cunningham J, Valery PC, Condon J, Roder D, et al., 'Reducing the burden of cancer for Aboriginal and Torres Strait Islander Australians: time for a coordinated, collaborative, priority-driven, Indigenous-led research program', Medical Journal of Australia, 194 530-531 (2011)
2011Chachay VS, Kirkpatrick CMJ, Hickman IJ, Ferguson M, Prins JB, Martin JH, 'Resveratrol - pills to replace a healthy diet?', BRITISH JOURNAL OF CLINICAL PHARMACOLOGY, 72 27-38 (2011)
DOI10.1111/j.1365-2125.2011.03966.xAuthor URL
CitationsScopus - 43Web of Science - 40
2011McGloughlin S, Roberts JA, O'Donoghue S, Martin J, Briscoe S, Lipman J, 'Ganciclovir pharmacokinetics and suggested dosing in continuous venovenous haemodiafiltration', INTERNATIONAL JOURNAL OF ANTIMICROBIAL AGENTS, 37 90-92 (2011)
DOI10.1016/j.ijantimicag.2010.10.003Author URL
CitationsScopus - 3Web of Science - 3
2011Martin JH, Kubler P, 'Treatment for pulmonary hypertension in Australia: too far too fast?', INTERNAL MEDICINE JOURNAL, 41 217-219 (2011)
DOI10.1111/j.1445-5994.2011.02437.xAuthor URL
CitationsScopus - 1Web of Science - 1
2011Martin JH, Fay MF, Udy A, Roberts J, Kirkpatrick C, Ungerer J, Lipman J, 'Pitfalls of using estimations of glomerular filtration rate in an intensive care population', INTERNAL MEDICINE JOURNAL, 41 537-543 (2011)
DOI10.1111/j.1445-5994.2009.02160.xAuthor URL
CitationsScopus - 24Web of Science - 20
2011Mcneill GBS, Martin JH, 'How reliable is eGFR when calculating drug dosage in acute medical admissions?', Internal Medicine Journal, 41 327-331 (2011)

Background: The Modification of Diet in Renal Disease-derived estimation of glomerular filtration rate (eGFR) is used widely. Although validated in stable chronic kidney disease (CKD) outpatients, it is not known how it performs in those presenting with acute medical illness. Aim: We aimed to compare eGFR with Cockroft Gault (CG) - the renal function assessment tool available prior to eGFR - to assess the difference in clinical outcome that would occur when one over another estimation is used in practice. In particular, we wished to assess whether use of eGFR would have resulted in a change of dose of commonly used acutely administered medications. Methods: Acute medical admissions presenting to a tertiary hospital between August and December 2008 were included. Serum creatinine concentration, age, sex, height and weight were collected. Renal function was estimated by both estimates. Movement from CKD class 3 to 4 or 5 was measured - a clinically used cut-off point for changes in management. Results: A total of 54 patients was included. eGFR values were higher than those estimated by CG. Almost half of patients categorized as CKD stage 4-5 using CG were only categorized as CKD stage 3 using eGFR. Conclusion: Although we did not use a gold standard estimation of GFR, this study shows that estimates of renal function vary in a clinically significant manner. As estimates of GFR are used to adjust drug dosages and to stratify for many other treatments, it is imperative that we find a method of estimating kidney function that is readily available, consistent and accurate. © 2011 The Authors. Internal Medicine Journal © 2011 Royal Australasian College of Physicians.

CitationsScopus - 2
2011Martin JH, Deacon CF, Gorrell MD, Prins JB, 'Incretin-based therapies - review of the physiology, pharmacology and emerging clinical experience', Internal Medicine Journal, 41 299-307 (2011)

Diabetes therapies based on manipulation of the incretin system are now widely available, with millions of people receiving treatment. The incretin hormones, glucose-dependent insulinotropic peptide and glucagon-like peptide-1 are released from endocrine cells in the small intestinal mucosa primarily in response to oral nutrient ingestion. They have various effects, but those most relevant to metabolic dysfunction include stimulation of insulin and suppression of glucagon secretion, with resultant reduction in fasting and postprandial glucose. Incretin secretion and/or action is impaired in type 2 diabetes, leading to development of strategies aimed at redressing this abnormality. These strategies include pharmacological inhibition of dipeptidyl peptidase-4, the enzyme responsible for the short half-life of endogenous incretins, and administration of long-acting dipeptidyl peptidase-4-resistant peptides that bind to and activate the glucagon-like peptide-1 receptor. In this review, we address aspects of incretin biology and pharmacotherapy with a view to highlighting potentially clinically relevant issues and areas of basic research that may impinge on these. © 2011 The Authors. Internal Medicine Journal © 2011 Royal Australasian College of Physicians.

CitationsScopus - 31
2010Jellis CL, Jenkins C, Leano R, Martin JH, Marwick TH, 'Reduced end-systolic pressure-volume ratio response to exercise: A marker of subclinical myocardial disease in type 2 diabetes', Circulation: Cardiovascular Imaging, 3 443-449 (2010)

Background-Limitations in the predictive value of negative exercise echocardiography in type 2 diabetes mellitus has been linked to a reduced end-systolic pressure-volume response (ESPVR). We sought whether abnormal ESPVR reflected subclinical diabetic heart disease by examining the association between the ESPVR and markers of myocardial dysfunction and to establish if the change (d) or peak systolic blood pressure/end-systolic left ventricular volume ratio (SP/ESV) is a better marker of contractile reserve in type 2 diabetes mellitus. Methods and Results-Resting and exercise echocardiography was performed in 167 apparently healthy patients with type 2 diabetes mellitus (97 men; age, 55±10 years) without ischemia, other cardiac disease, or noncardiac complications of diabetes. Standard echocardiographic and color tissue Doppler measures (early diastolic tissue velocity, strain, and strain rate) were acquired at baseline and peak stress in apical long-axis views. Calibrated integrated backscatter was calculated from a resting parasternal long-axis view. dSP/ESV was calculated as [(peak stress SP/ESV)-(rest SP/ESV)]. The 83 subjects who demonstrated a dSP/ESV =12 mm Hg/mL/m2 after exercise were older and had lower peak heart rate, resting diastolic and stress systolic tissue velocity, stress ejection fraction, and exercise capacity than the remainder. There was no significant association between dSP/ESV and metabolic derangement or echocardiographic measures of deformation or backscatter. Change in Sm and stress ejection fraction were independent correlates of dSP/ESV. Conclusions-dSP/ESV ratio is associated with established features of subclinical diabetic heart disease as well as determinants of contractile reserve (peak hemodynamic response and stress systolic function). Peak ESPVR is poorly associated with markers of myocardial dysfunction. © 2010 American Heart Association, Inc.

CitationsScopus - 6
2010Martin JH, Norris R, Barras M, Roberts J, Morris R, Doogue M, Jones GRD, 'Guidelines Review - Therapeutic monitoring of vancomycin in adult patients: A consensus review of the American Society of Health-System Pharmacists, the Infectious Diseases Society of America, and the Society of Infectious Diseases Pharmacists', Clinical Biochemist Reviews, 31 21-24 (2010)
2010Martin JH, Avent M, Pattullo C, Dines A, Kubler P, 'Drug Use Evaluation Services in Australia and New Zealand: A Neglected Area of Research?', J Pharm Pract Res, 40 15-18 (2010)
2010Martin JH, Jellis CL, Narula J, Markwick TH, 'Assessment of nonischemic myocardial fibrosis', J. Am. Coll. Cardiol, 56 89-97 (2010)
2010Martin JH, Jellis CL, Stanton T, Leano R, Markwick TH, 'Subclinical myocardial disease in type 2 diabetes: Mechanistic insights from resting and exercise haemodynamics', Heart Lung and Circulation, 19 S196 (2010)
2010Phillips LK, Peake JM, Zhang X, Hickman IJ, Kolade O, Sacre JW, et al., 'The effect of a high-fat meal on postprandial arterial stiffness in men with obesity and type 2 diabetes', Journal of Clinical Endocrinology and Metabolism, 95 4455-4459 (2010)

Context: Postprandial dysmetabolism is emerging as an important cardiovascular risk factor. Augmentation index (AIx) is a measure of systemic arterial stiffness and independently predicts cardiovascular outcome. Objective: The objective of this study was to assess the effect of a standardized high-fat meal on metabolic parameters and AIx in 1) lean, 2) obese nondiabetic, and 3) subjects with type 2 diabetes mellitus (T2DM). Design and Setting: Male subjects (lean, n = 8; obese, n = 10; and T2DM, n = 10) were studied for 6 h after a high-fat meal and water control. Glucose, insulin, triglycerides, and AIx (radial applanation tonometry) were measured serially to determine the incremental area under the curve (iAUC). Results: AIx decreased in all three groups after a high-fat meal. A greater overall postprandial reduction in AIx was seen in lean and T2DM compared with obese subjects (iAUC, 2251 ± 1204, 2764 ± 1102, and 1187 ± 429% · min, respectively; P < 0.05). The time to return to baseline AIx was significantly delayed in subjects with T2DM (297 ± 68 min) compared with lean subjects (161 ± 88 min; P < 0.05). There was a significant correlation between iAUC AIx and iAUC triglycerides (r = 0.50; P < 0.05). Conclusions: Obesity is associated with an attenuated overall postprandial decrease in AIx. Subjects with T2DM have a preserved, but significantly prolonged, reduction in AIx after a high-fat meal. The correlation between AIx and triglycerides suggests that postprandial dysmetabolism may impact on vascular dynamics. The markedly different response observed in the obese subjects compared with those with T2DM was unexpected and warrants additional evaluation. Copyright © 2010 by The Endocrine Society.

CitationsScopus - 11
2010Martin JH, Norris R, Barras M, Roberts J, Morris R, Doogue M, Jones GR, 'Therapeutic monitoring of vancomycin in adult patients: a consensus review of the American Society of Health-System Pharmacists, the Infectious Diseases Society of America, and the Society Of Infectious Diseases Pharmacists.', The Clinical biochemist. Reviews / Australian Association of Clinical Biochemists, 31 21-24 (2010)
2010Norris RL, Martin JH, Thompson E, Ray JE, Fullinfaw RO, Joyce D, et al., 'Current Status of Therapeutic Drug Monitoring in Australia and New Zealand: A Need for Improved Assay Evaluation, Best Practice Guidelines, and Professional Development', THERAPEUTIC DRUG MONITORING, 32 615-623 (2010)
DOI10.1097/FTD.0b013e3181ea3e8aAuthor URL
CitationsScopus - 10Web of Science - 10
2010Martin JH, Connelly KA, Boyle A, Kompa A, Zhang Y, Kelly D, et al., 'Effect of Atorvastatin on Cardiac Remodelling and Mortality in Rats Following Hyperglycemia and Myocardial Infarction', INTERNATIONAL JOURNAL OF CARDIOLOGY, 143 353-360 (2010) [C1]
DOI10.1016/j.ijcard.2009.03.098Author URL
CitationsScopus - 3Web of Science - 2
Co-authorsAndrew Boyle
2010Protani M, Coory M, Martin JH, 'Effect of obesity on survival of women with breast cancer: Systematic review and meta-Analysis', Breast Cancer Research and Treatment, 123 627-635 (2010)

Obesity is a risk factor for the development of new cases of breast cancer and also affects survival in women who have already been diagnosed with breast cancer. Early studies of obesity and breast cancer survival have been summarised in two meta-Analyses, but the latest of these only included studies that recruited women diagnosed as recently as 1991. The primary aim of this study was to conduct a meta-Analysis that included the more recent studies. A systematic search of MEDLINE, EMBASE and CINAHL was conducted to identify original data evaluating the effects of obesity on survival in newly diagnosed breast cancer patients. Adjusted hazard ratios (HR) from individual studies were pooled using a random effects model. A series of pre-specified sensitivity analyses were conducted on factors such as overall versus breast cancer survival and treatment versus observational cohort. The meta-Analysis included 43 studies that enrolled women diagnosed with breast cancer between 1963 and 2005. Sample size ranged from 100 to 424168 (median 1192). The meta-Analysis showed poorer survival among obese compared with nonobese women with breast cancer, which was similar for overall (HR = 1.33; 95% confidence interval (CI): 1.21, 1.47) and breast cancer specific survival (HR = 1.33; 95% CI: 1.19, 1.50). The survival differential varied only slightly, depending on whether body mass index (1.33; 1.21, 1.47) or waist-hip ratio (1.31; 1.08, 1.58) was used as the measure of obesity. There were larger differences by whether the woman was pre-menopausal (1.47) or post-menopausal (1.22); whether the cohort included women diagnosed before (1.31) or after 1995 (1.49); or whether the women were in a treatment (1.22) or observational cohort (1.36), but none of the differences were statistically significant. Women with breast cancer, who are obese, have poorer survival than women with breast cancer, who are not obese. However, no study has elucidated the causal mechanism and there is currently no evidence that weight loss after diagnosis improves survival. Consequently, there is currently no reason to place the additional burden of weight loss on women already burdened with a diagnosis of cancer. Further research should concentrate on assessing whether factors such as diabetes or type of chemotherapy modify the obesity effect and on understanding the causal mechanism, in particular the role of relative under-dosing. © Springer Science+Business Media, LLC. 2010.

CitationsScopus - 203
2010Hollingworth S, Duncan EL, Martin JH, 'Marked increase in proton pump inhibitors use in Australia', Pharmacoepidemiology and Drug Safety, 19 1019-1024 (2010)

Objectives: To examine the trends in the prescribing of subsidised proton pump inhibitors (PPIs) and histamine receptor antagonists (H2RAs), in the Australian population from 1995 to 2006 to encourage discussion regarding appropriate clinical use. PPIs and H2RAs are the second highest drug cost to the publicly subsidised Pharmaceutical Benefits Scheme (PBS). Design: Government data on numbers of subsidised scripts, quantity and doses for PPIs and H2RAs were analysed by gender and age, dose and indication. Main outcome measure: Drug utilisation as DDD [defined daily dose]/1000 population/day. Results: The use of combined PPIs increased by 1318%. Utilisation increased substantially after the relaxation of the subsidised indications for PPIs in 2001. Omeprazole had the largest market share but was substituted by its S-enantiomer esomeprazole after its introduction in 2002. There was considerable use in the elderly with the peak use being in those aged 80 years and over. The utilisation of H2RAs declined 72% over 12 years. Conclusions: PPI use has increased substantially, not only due to substitution of H2RAs but to expansion in the overall market. Utilisation does not appear to be commensurate with prevalence of gastro-oesophageal reflux disease (GORD) nor with prescribing guidelines for PPIs, with significant financial costs to patients and PBS. This study encourages clinical discussion regarding quality use of these medicines. © 2010 John Wiley & Sons, Ltd.

CitationsScopus - 23
2010Scott KA, Martin JH, Inder WJ, 'Acidosis in the hospital setting: is metformin a common precipitant?', INTERNAL MEDICINE JOURNAL, 40 342-346 (2010)
DOI10.1111/j.1445-5994.2009.01959.xAuthor URL
CitationsScopus - 8Web of Science - 8
2010Martin JH, Fay MF, 'Surrogate end-points in clinical practice: are we providing worse care?', INTERNAL MEDICINE JOURNAL, 40 395-398 (2010)
DOI10.1111/j.1445-5994.2010.02248.xAuthor URL
CitationsScopus - 4Web of Science - 4
2010Doogue MP, Martin JH, 'Editorial: Whither therapeutic drug monitoring?', Internal Medicine Journal, 40 671-672 (2010)
2010Siriwardane D, Woodman R, Hakendorf P, Martin JH, White GH, Ben-Tovim DI, Thompson CH, 'Stability of plasma creatinine concentrations in acute complex long-stay admissions to a general medical service', Clinical Medicine, Journal of the Royal College of Physicians of London, 10 540-543 (2010)

Assessment of glomerular filtration rate (GFR) is essential for calculating safe dosages of renally cleared drugs. Formulae for estimating reliable GFRs assume that plasma creatinine concentrations are stable. This study evaluates the variability of plasma creatinine (PCr) concentrations in patients admitted acutely to hospital. From 2,293 newly admitted patients, those in whom a subsequent clinically significant change (>20%) in PCr had occurred were identified. Median age was 81.1 years. Median baseline PCr was 90 umol/l (eGFR 60 ml/min). In total, 46.3% of the patients had a PCr that varied >20% from baseline three to seven days following admission. A 10-year increase in age increased the odds of a rise in PCr over the next week by 11.1% (odds ratio=1.11, 95% confidence interval=1.03, 1.20; p=0.007). Overall, baseline creatinine was a poor predictor of subsequent variation in PCr. GFR formulae for calculating renally-cleared drug dosages should be used with caution in elderly patients admitted acutely to hospital. © Royal College of Physicians, 2010. All rights reserved.

CitationsScopus - 4
2009Howell S, Coory M, Martin J, Duckett S, 'Using routine inpatient data to identify patients at risk of hospital readmission', BMC HEALTH SERVICES RESEARCH, 9 (2009)
DOI10.1186/1472-6963-9-96Author URL
CitationsScopus - 31Web of Science - 29
2009Martin JH, Mangiafico S, Kelly DJ, 'Role of statins in diabetes complications', Current Diabetes Reviews, 5 165-170 (2009)

Diabetes is one of the major causes of morbidity and mortality in the Western world and it currently affects 35 million people in the US alone. Cardiovascular and renal complications of diabetes, Type I and II, account for much of this morbidity, and are now known to be the end result of a complex interplay of pathophysiological processes. These include haemodynamic and metabolic abnormalities such as endothelial dysfunction, inflammation, vasoconstriction, oxidation and fibrosis. For some time it has been difficult to elucidate whether these processes and subsequent dysfunction in organs such as the heart and kidney is due to processes that often coexist with diabetes, such as hypertension. However, it is now clear that there is a distinct pro-inflammatory and pro-fibrotic state in diabetes, which may in addition be complicated by synergistic disease processes. The use of statins in diabetes has been of interest for a while due to the known effect of statins on inflammatory and fibrotic pathways. This review covers the clinical evidence for the use of statins in diabetes, the major known pathophysiological processes that occur in diabetic organ disease and discusses the known and putative effects of statins on these pathways. It concludes with a brief discussion of some early and yet unpublished work regarding the addition of statin therapy to angiotensin inhibition therapy in diabetic disease. © 2009 Bentham Science Publishers Ltd.

CitationsScopus - 6
2009Martin JH, 'Advances in anticoagulants', Australian Doctor, . (2009)
2009Martin JH, Doogue M, Somogyi A, Miners J, 'Prescribing in liver disease. Letter in response to Australian Prescriber', Australian Prescriber, 32 32(2):32-35 & 32(5):120 (2009)
2009Martin JH, Doogue M, 'Editorial ¿ Guidelines or external regulation?', Internal Medicine Journal, 39 789-791 (2009)
2009Martin JH, Ghiculescu A, 'Rapidly Progressive Severe Amiodarone-induced Hypothyroidism in an Elderly Female', Journal of Pharmacy Practice and Research, 39 140-141 (2009)
2009Martin JH, Morris R, Beer C, Doogue M, 'Doctors and the pharmaceutical industry: time for a national policy?', Medical Journal of Australia, 191 189-190 (2009)
2009Martin JH, Fay MF, Ungerer JP, 'eGFR - use beyond the evidence', MEDICAL JOURNAL OF AUSTRALIA, 190 197-199 (2009)
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CitationsScopus - 13Web of Science - 11
2009Sweidan M, Reeve JF, Brien J-AE, Jayasuriya P, Martin JH, Vernon GM, 'Quality of drug interaction alerts in prescribing and dispensing software', MEDICAL JOURNAL OF AUSTRALIA, 190 251-254 (2009)
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CitationsScopus - 30Web of Science - 27
2009Martin JH, Beer C, Morris RG, Doogue MP, 'Doctors and the pharmaceutical industry: time for a national policy?', MEDICAL JOURNAL OF AUSTRALIA, 191 189-190 (2009)
Author URL
2009Sweidan M, Reeve JF, Brien J-AE, Jayasuriya P, Martin JH, Vernon GM, 'Quality of drug interaction alerts in prescribing and dispensing software REPLY', MEDICAL JOURNAL OF AUSTRALIA, 191 358-359 (2009)
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2009Martin JH, 'Pharmacogenetics of warfarin - is testing clinically indicated?', AUSTRALIAN PRESCRIBER, 32 76-80 (2009)
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CitationsScopus - 5Web of Science - 4
2009Doogue M, Martin J, Miners J, Somogyi A, 'Prescribing in liver disease', AUSTRALIAN PRESCRIBER, 32 120-120 (2009)
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2009Martin JH, Coory MD, Valery PC, Green AC, 'Association of diabetes with survival among cohorts of Indigenous and non-Indigenous Australians with cancer', CANCER CAUSES & CONTROL, 20 355-360 (2009)
DOI10.1007/s10552-008-9249-zAuthor URL
CitationsScopus - 6Web of Science - 7
2009Martin JH, Woods M, Mudge A, 'Old bugs new populations: an unusual presentation of pericarditis', INTERNAL MEDICINE JOURNAL, 39 850-851 (2009)
DOI10.1111/j.1445-5994.2009.02079.xAuthor URL
CitationsScopus - 1Web of Science - 1
2008Martin J, 'Statins and Congestive Heart Failure', CURRENT ATHEROSCLEROSIS REPORTS, 10 369-376 (2008)
DOI10.1007/s11883-008-0058-3Author URL
CitationsScopus - 1Web of Science - 1
2008Martin JH, Norris RL, Morris RG, Ray JE, Fullinfaw RO, Ilett KF, et al., 'A survey of Therapeutic Drug Monitoring in Australia and New Zealand', Clinical Biochemist Reviews, 29 Supp (iii) (2008)
2007Kelly DJ, Zhang Y, Connelly K, Cox AJ, Martin J, Krum H, Gilbert RE, 'Tranilast attenuates diastolic dysfunction and structural injury in experimental diabetic cardiomyopathy', AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY, 293 H2860-H2869 (2007)
DOI10.1152/ajpheart.01167.2006Author URL
CitationsWeb of Science - 27
2007Martin JH, Connelly K, Kelly D, Zhang Y, Prior D, Cox A, et al., 'Functional, structural and molecular aspects of diastolic heart failure in the diabetic (mRen202) 27 rat', Cardiovascular Research, 76 280-291 (2007)
2007Martin JH, Krum H, 'Statins and clinical outcomes in heart failure', CLINICAL SCIENCE, 113 119-127 (2007)
DOI10.1042/CS20070031Author URL
CitationsScopus - 20Web of Science - 17
2007Connelly KA, Kelly DJ, Martin JH, Zhang Y, Thai K, Krum H, Gilbert RE, 'Hyperglycaemia and an enhanced tissue RAS are necessary components in the pathogenesis of diabetic cardiac microvascular complications, mediated via PKC beta isoform', EUROPEAN HEART JOURNAL, 28 550-550 (2007)
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2005Martin JH, Kelly DJ, Mifsud SA, Zhang Y, Cox AJ, See F, et al., 'Tranilast attenuates cardiac matrix deposition in experimental diabetes: role of transforming growth factor-B¿', Cardiovascular Research, 65 694-701 (2005)
2005Martin JH, Denver R, Bailey M, Krum H, 'In Vitro inhibitory effects of atorvastatin on cardiac fibroblasts: implications for ventricular remodelling', Clinical and Experimental Pharmacology and Physiology, 32 697-701 (2005)
2005Martin JH, See F, Kompa A, Lewis DA, Krum H, 'Fibrosis as a Therapeutic Target Post-Myocardial Infarction. Current Pharmaceutical Design', Current Pharmaceutical Design, 11 477-487 (2005)
2003Martin JH, Liew D, Krum H, 'Eplerenone (Pharmacia)', Curr Opin Investig Drugs, 4 316-322 (2003)
2003Martin J, Krum H, 'Cytochrome P450 drug interactions within the HMG-CoA reductase inhibitor class - Are they clinically relevant?', DRUG SAFETY, 26 13-21 (2003)
DOI10.2165/00002018-200326010-00002Author URL
CitationsScopus - 45Web of Science - 36
2003Martin JH, Mourton SM, Nicholls MG, 'Severe hyperkalaemia with prescription of potassium-retaining agents in an elderly patient', New Zealand Medical Journal, 116 (2003)
CitationsScopus - 2
2002Berakis A, Williams TJ, Naughton MT, Martin JH, Muhlmann M, Krum H, 'Altered sympathetic and parasympathetic activity in lung transplantation patients at rest and following autonomic perturbation', CHEST, 122 1192-1199 (2002)
DOI10.1378/chest.122.4.1192Author URL
CitationsScopus - 14Web of Science - 12
2001Martin JH, Begg EJ, Kennedy MA, Roberts R, Barclay ML, 'Is cytochrome P4502C9 genotype associated with NSAID gastric ulceration?', BRITISH JOURNAL OF CLINICAL PHARMACOLOGY, 51 627-630 (2001)
DOI10.1046/j.0306-5251.2001.01398.xAuthor URL
CitationsScopus - 40Web of Science - 36
2001Martin JH, 'Cytochrome P450 drug interactions: are they clinically relevent?', Australian Prescriber, 24 10-12 (2001)
2001Martin JH, 'Cytochrome P450 drug interactions', Australian Prescriber, 24 80-81 (2001)
2001Martin JH, 'Eplerenone (GD Searle)', Current Opinion Invest Drugs, 2 521-524 (2001)
2001Martin JH, Fay MF, 'Capecitabine', Current Therapeutics, 42 49-51 (2001)
2001Martin JH, 'The Heart Failure Journal Club: a review of publications on heart failure in American Heart Journal', Eur J Heart Failure, 3 125-137 (2001)
2001Martin JH, 'Diltiazem-mediated inhibition of sildenafil metabolism may promote nitrate-induced hypotension', Internal Medicine Journal, 31 374-374 (2001)
2001Martin JH, 'Role of valsartan and other angiotensin receptor blocking agents in the management of cardiovascular disease', Pharmacological Research, 46 203-212 (2001)
2000Martin JH, 'Drug prices not the whole story', Medical Observer, Melbourne, 24-24 (2000)
2000Martin JH, Begg EJ, 'Reference pricing - is it in the public interest?', New Zealand Medical Journal, 113 422-425 (2000)
1999Martin JH, Begg EJ, 'OC'S - emotional journalism?', GP Weekly, . (1999)
1995Martin JH, Abbott G, 'Serum sickness-like illness and antimicrobials in children', New Zealand Medical Journal, 108 123-124 (1995)
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Review (1 outputs)

2013, 'Reviewer', Essentials of Internal Medicine, 3rd Edition (2013)

Conference (8 outputs)

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2009Norris R, Morris R, Thompson E, Ray J, Barras M, Jones G, Martin J, 'A Survey of Therapeutic Drug Monitoring in Australasia', THERAPEUTIC DRUG MONITORING, Montreal, CANADA (2009)
Author URL
2006Martin JH, Connelly K, Boyle A, Kelly DJ, Kompa A, Zhang M, et al., 'Hyperglycemia has a detrimental effect on cardiac remodelling and mortality after myocardial infarction: benefit of statin therapy', EUROPEAN HEART JOURNAL, Barcelona, SPAIN (2006)
Author URL
CitationsWeb of Science - 1
2004Martin JH, Kelly D, Misfud S, Zhang M, Krum H, Wilkinson-Berka J, Gilbert R, 'Tranilast dose-dependently attenuates extra-cellular matrix deposition in rats.', CLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Glasgow, SCOTLAND (2004)
Author URL
2003Martin JH, Denver R, Pepe S, Krum H, 'Direct, dose-dependent anti-fibrotic effects of atorvastatin in rat and human cardiac fibroblast cell culture', EUROPEAN HEART JOURNAL, VIENNA, AUSTRIA (2003)
DOI10.1016/S0195-668X(03)95164-5Author URL
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Research Supervision

Current Supervision

CommencedResearch Title / Program / Supervisor Type
2015Developmental and Environmental Determinants on Neonatal Pharmacology
Pharmacology, Faculty of Health and Medicine
2015Pharmacokinetics and Pharmacodynamics of Synthetic Cannabinoids in Humans
Pharmacology, Faculty of Health and Medicine
Principal Supervisor
2014Pharmacovigilance of immunology medications
Pharmacology, University of Queensland
2014Combined pharmacogenetics and kinetics in hematology
Pharmacology, University of Queensland
Pharmacology, University of Queensland
Pharmacology, University of Queensland
2012Effect of obesity on mortality in breast cancer
Pharmacology, University of Queensland
Principal Supervisor
2012Helping students structure knowledge for clinical use in PBL
Pharmacology, University of Queensland
Consultant Supervisor
2010Combined effect of diabetes and obesity on survival in cancer
Pharmacology, University of Queensland
2010The role of resveratrol, a polyphenolic compound found in red grape skin, in the management of non-alcoholic fatty liver disease
Pharmacology, University of Queensland

Professor Jennifer Martin


Chair of Clinical Pharmacology
School of Medicine and Public Health
School of Medicine and Public Health
Faculty of Health and Medicine

Contact Details
Phone(02) 4921 1286
Fax(02) 4960 2088


RoomCalvary Mater Hospital, Newmed 2, Room 5.35
BuildingNewmed 2
LocationCalvary Mater Hospital