Dr Christopher Rowe
School of Medicine and Public Health
I am an Adult Endocrinologist (Fellow of the Royal Australasian College of Physicians), with practice at John Hunter Hospital and at Newcastle Endocrinology, as well as Clinical Lecturer at the University of Newcastle.
I have recently returned from a visiting Fellowship to the Institute of Metabolism and Systems Research at the University of Birmingham and Queen Elizabeth Hospital, with Professor Chris McCabe and Dr Kristien Boelaert.
My primary area of research relates to thyroid nodules and thyroid cancer, although I am active across a wide range of projects in diabetes, pregnancy and endocrinology in the basic and clinical spheres.
My current doctoral studies through the University of Newcastle School of Medicine and Public Health are investigating new diagnostic and therapetic targets for thyroid cancer. In particular, our group is examining the utility of the TSH receptor as a specific theranostic marker for drug delivery, in collaboration with the John Hunter Hospital Thyroid Cancer Multidisciplinary Team, the Hunter Cancer Biobank and Pathology North (Hunter). I am also collaborating with Professor Hubert Hondermarck in the School of Biomedical Sciences and Pharmacy to study the role of neurotrophins as biomarkers and therapeutic targets in thyroid malignancy.
I am active in a number of clinical research projects studying the impact of visceral fat on insulin resistance in Type 1 Diabetes, and management of diabetes in pregnancy.
I am an inaugural recipient of a Clinical Research Fellowship (Hunter New England Local Health District), and my recent research has been supported by the Hunter Cancer Research Alliance, Avant Mutual Group, the University of Newcastle, and the John Hunter Hospital Charitable Trust.
- Bachelor of Medicine, Bachelor of Surgery (Hons), University of New South Wales
- Bachelor of Science (Medicine), University of New South Wales
- Diabetes Mellitus
- insulin resistance
Fields of Research
|110901||Autonomic Nervous System||20|
|110102||Medical Biochemistry: Carbohydrates||20|
|Title||Organisation / Department|
|Lecturer||University of Newcastle
School of Medicine and Public Health
ADIPS Outstanding Abstract Award (Travel Grant)
Australasian Diabetes in Pregnancy Society
Australian Diabetes Society Travel Grant (Outstanding Abstract)
Australian Diabetes Society (ADS)
Australasian Diabetes in Pregnancy Society Travel Grant (Outstanding Abstract)
Australian Diabetes in Pregnancy Society (ADIPS)
Endocrine Society (USA) Travel Grant (Outstanding Abstract)
The Endocrine Society
|Year||Title / Rationale|
Maternal hyperglycaemia and neonatal hypoglycaemia following betamethasone can be safely reduced by a pregnancy-specific algorithm-driven intravenous insulin infusion in women with gestational diabetes
For publications that are currently unpublished or in-press, details are shown in italics.
Chapter (1 outputs)
Rowe C, Boelaert K, Smith R, 'Thyroid Cancer During Pregnancy and Lactation', Maternal-Fetal and Neonatal Endocrinology: Physiology, Pathophysiology, and Clinical Management, Academic Press: Elsevier, United States of America 317-327 (2019)
Journal article (9 outputs)
Rowe CW, Arthurs S, O Neill CJ, Hawthorne J, Carroll R, Wynne K, Bendinelli C, 'High-dose preoperative cholecalciferol to prevent post-thyroidectomy hypocalcaemia: A randomized, double-blinded placebo-controlled trial', Clinical Endocrinology, 90 343-350 (2019) [C1]
© 2018 John Wiley & Sons Ltd. Objective: Post-thyroidectomy hypocalcaemia is a significant cause of morbidity and prolonged hospitalization, usually due to transient parathy... [more]
© 2018 John Wiley & Sons Ltd. Objective: Post-thyroidectomy hypocalcaemia is a significant cause of morbidity and prolonged hospitalization, usually due to transient parathyroid gland damage, treated with calcium and vitamin D supplementation. We present a randomized, double-blinded placebo-controlled trial of preoperative loading with high-dose cholecalciferol (300¿000 IU) to reduce post-thyroidectomy hypocalcaemia. Patients and Measurements: Patients (n¿=¿160) presenting for thyroidectomy at tertiary hospitals were randomized 1:1 to cholecalciferol (300¿000¿IU) or placebo 7¿days prior to thyroidectomy. Ten patients withdrew prior to surgery. The primary outcome was post-operative hypocalcaemia (corrected calcium <2.1¿mmol/L in first 180¿days). Results: The study included 150 patients undergoing thyroidectomy for Graves¿ disease (31%), malignancy (20%) and goitre (49%). Mean pre-enrolment vitamin D was 72¿±¿26¿nmol/L. Postoperative hypocalcaemia occurred in 21/72 (29%) assigned to cholecalciferol and 30/78 (38%) participants assigned to placebo (P¿=¿0.23). There were no differences in secondary end-points between groups. In pre-specified stratification, baseline vitamin D status did not predict hypocalcaemia, although most individuals were vitamin D replete at baseline. Post-hoc stratification by day 1 parathyroid hormone (PTH) (<10¿pg/mL, low vs =10¿pg/mL, normal) was explored due to highly divergent rates of hypocalcaemia in these groups. Using a Cox regression model, the hazard ratio for hypocalcaemia in the cholecalciferol group was 0.56 (95%CI 0.32-0.98, P¿=¿0.04) after stratification for Day 1 PTH. Further clinical benefits were observed in these subgroups. Conclusions: Pre-thyroidectomy treatment with high-dose cholecalciferol did not reduce the overall rate of hypocalcaemia following thyroidectomy. In subgroups stratified by day 1 PTH status, improved clinical outcomes were noted.
Rowe CW, Putt E, Brentnall O, Gebuehr A, Allabyrne J, Woods A, Wynne K, 'An intravenous insulin protocol designed for pregnancy reduces neonatal hypoglycaemia following betamethasone administration in women with gestational diabetes', Diabetic Medicine, 36 228-236 (2019) [C1]
© 2018 Diabetes UK Aims: Marked hyperglycaemia is common following betamethasone administration in women with gestational diabetes (GDM), and may contribute to neonatal hypoglycae... [more]
© 2018 Diabetes UK Aims: Marked hyperglycaemia is common following betamethasone administration in women with gestational diabetes (GDM), and may contribute to neonatal hypoglycaemia. Validated protocols to deliver glycaemic stability following betamethasone are lacking. We hypothesized that an intravenous insulin (IVI) protocol for pregnancy-specific glycaemic targets (Pregnancy-IVI) would achieve greater at-target glycaemic control than a generic adult intravenous insulin protocol (Adult-IVI), and may reduce neonatal hypoglycaemia. Methods: A retrospective cohort study of the performance Adult-IVI and Pregnancy-IVI following betamethasone in GDM, sequentially implemented at a tertiary hospital, without change in indication for IVI. Cases were identified by electronic record search. Primary outcome was percentage of on-IVI time with at-target glycaemia [blood glucose level (BGL) 3.8¿7¿mmol/l]. Secondary outcomes were time with critical hyperglycaemia (BGL >¿10¿mmol/l), occurrence of maternal hypoglycaemia (BGL <¿3.8¿mmol/l), and incidence of neonatal hypoglycaemia (BGL =¿2.5¿mmol/l) if betamethasone was administered within 48¿h of birth. Results: The cohorts comprised 151 women (Adult-IVI n¿=¿86; Pregnancy-IVI n¿=¿65). The primary outcome was 68% time-at-target [95% confidence interval (CI) 64¿71%) for Pregnancy-IVI compared with 55% (95% CI 50¿60%) for Adult-IVI (P¿=¿0.0002). Critical maternal hyperglycaemia (0% vs. 2%, P¿=¿0.02) and hypoglycaemia (2% vs. 12%, P¿=¿0.02) were both lower with Pregnancy-IVI than Adult-IVI. Neonatal hypoglycaemia was less common after Pregnancy-IVI (29%) than after Adult-IVI (54%, P¿=¿0.03). A multiple logistic regression model adjusting for potential confounders gave an odds ratio for neonatal hypoglycaemia with Pregnancy-IVI of 0.27 (95% CI 0.10¿0.76, P¿=¿0.01). Conclusions: An IVI protocol designed for pregnancy effectively controlled maternal hyperglycaemia following betamethasone administration in GDM. This is the first intervention to show a reduction in betamethasone-associated neonatal hypoglycaemia, linked with optimum maternal glycaemic control.
Marlow AL, Rowe CW, Anderson D, Wynne K, King BR, Howley P, Smart CE, 'Young children, adolescent girls and women with type 1 diabetes are more overweight and obese than reference populations, and this is associated with increased cardiovascular risk factors.', Diabetic medicine : a journal of the British Diabetic Association, 36 1487-1493 (2019) [C1]
Gao F, Griffin N, Faulkner S, Rowe CW, Williams L, Roselli S, et al., 'The neurotrophic tyrosine kinase receptor TrkA and its ligand NGF are increased in squamous cell carcinomas of the lung', SCIENTIFIC REPORTS, 8 (2018) [C1]
Faulkner S, Jobling P, Rowe CW, Rodrigues Oliveira SM, Roselli S, Thorne RF, et al., 'Neurotrophin Receptors TrkA, p75
© 2018 American Society for Investigative Pathology Neurotrophin receptors are emerging targets in oncology, but their clinicopathologic significance in thyroid cancer is unclear.... [more]
© 2018 American Society for Investigative Pathology Neurotrophin receptors are emerging targets in oncology, but their clinicopathologic significance in thyroid cancer is unclear. In this study, the neurotrophin tyrosine receptor kinase TrkA (also called NTRK1), the common neurotrophin receptor p75NTR, and the proneurotrophin receptor sortilin were analyzed with immunohistochemistry in a cohort of thyroid cancers (n = 128) and compared with adenomas and normal thyroid tissues (n = 62). TrkA was detected in 20% of thyroid cancers, compared with none of the benign samples (P = 0.0007). TrkA expression was independent of histologic subtypes but associated with lymph node metastasis (P = 0.0148), suggesting the involvement of TrkA in tumor invasiveness. Nerves in the tumor microenvironment were positive for TrkA. p75NTR was overexpressed in anaplastic thyroid cancers compared with papillary and follicular subtypes (P < 0.0001). Sortilin was overexpressed in thyroid cancers compared with benign thyroid tissues (P < 0.0001). Neurotrophin receptor expression was confirmed in a panel of thyroid cancer cell lines at the mRNA and protein levels. Functional investigations using the anaplastic thyroid cancer cell line CAL-62 found that siRNA against TrkA, p75NTR, and sortilin decreased cell survival and cell migration through decreased SRC and ERK activation. Together, these data reveal TrkA, p75NTR, and sortilin as potential therapeutic targets in thyroid cancer.
Rowe CW, Paul JW, Gedye C, Tolosa JM, Bendinelli C, McGrath S, Smith R, 'Targeting the TSH receptor in thyroid cancer', Endocrine-Related Cancer, 24 R191-R202 (2017) [C1]
© 2017 Society for Endocrinology Printed in Great Britain. Recent advances in the arena of theranostics have necessitated a re-examining of previously established fields. The exis... [more]
© 2017 Society for Endocrinology Printed in Great Britain. Recent advances in the arena of theranostics have necessitated a re-examining of previously established fields. The existing paradigm of therapeutic thyroid-stimulating hormone receptor (TSHR) targeting in the post-surgical management of differentiated thyroid cancer using levothyroxine and recombinant human thyroid-stimulating hormone (TSH) is well understood. However, in an era of personalized medicine, and with an increasing awareness of the risk profile of longstanding pharmacological hyperthyroidism, it is imperative clinicians understand the molecular basis and magnitude of benefit for individual patients. Furthermore, TSHR has been recently re-conceived as a selective target for residual metastatic thyroid cancer, with pilot data demonstrating effective targeting of nanoparticles to thyroid cancers using this receptor as a target. This review examines the evidence for TSHR signaling as an oncogenic pathway and assesses the evidence for ongoing TSHR expression in thyroid cancer metastases. Priorities for further research are highlighted.
Rowe CW, Haider AS, Viswanathan D, Jones M, Attia J, Wynne K, Acharya S, 'Insulin resistance correlates with maculopathy and severity of retinopathy in young adults with Type 1 Diabetes Mellitus', Diabetes Research and Clinical Practice, 131 154-160 (2017) [C1]
© 2017 Elsevier B.V. Aims To assess the relationship between insulin resistance (IR), retinopathy and maculopathy in young adults with Type 1 diabetes mellitus. Methods A cross-se... [more]
© 2017 Elsevier B.V. Aims To assess the relationship between insulin resistance (IR), retinopathy and maculopathy in young adults with Type 1 diabetes mellitus. Methods A cross-sectional study at a regional Australian tertiary hospital. Retinal pathology, assessed by colour fundus photography, was correlated with two surrogate measures of IR: estimated Glucose Disposal Rate (eGDR) and Insulin Sensitivity Score (ISS), where lower scores reflect greater IR. Results 107 patients were recruited, with mean age 24.7¿years, 53% male, and mean duration of disease 10.8¿years. Mean eGDR scores (5.6¿vs 8.0 p¿<¿0.001) and ISS (4.7¿vs 7.9, p¿<¿0.001) were lower in subjects having at least moderate non-proliferative diabetic retinopathy (NPDR; relative to nil/mild-NPDR). Similarly, mean eGDR (4.2¿vs 6.2, p¿=¿0.001) and ISS (3.8¿vs 6.1, p¿=¿0.003) were lower in patients with maculopathy. Multivariate logistic regression modelling was used to control for confounding. For retinopathy severity, a unit increase in eGDR or ISS (representing lower IR) was associated with a 50% decrease in odds of moderate-NPDR or worse (eGDR OR 0.5, 95%CI 0.32¿0.77, p¿=¿0.002; ISS OR 0.49, 95%CI 0.29¿0.84, p¿=¿0.01). A unit increase in eGDR or ISS was associated with a 46¿56% decrease in odds of maculopathy (eGDR OR 0.54, 95%CI 0.37¿0.81, p¿=¿0.003; ISS OR 0.44, 95%CI 0.22¿0.88, p¿=¿0.02). Conclusions IR correlates with more severe retinopathy in young adults with Type 1¿DM. This is the first description of a correlation between IR and maculopathy in Type 1¿DM, warranting further evaluation. Prospective studies examining whether reducing IR can improve microvascular complications are required.
|Show 6 more journal articles|
Conference (24 outputs)
Rowe C, Woods A, Wynne K, 'Transient extreme insulin resistance in pregnancy following betamethasone administration managed with high-dose intravenous insulin: case series and literature review.', Sydney, Australia (2019)
Rowe C, Delbridge M, Brown K, Watkins B, Addley J, Wynne K, 'An insulin infusion designed for pregnancy provides comparable glycaemic control following betamethasone in women with gestational and pre-existing diabetes, although hypoglycaemia is more common in pre-existing diabetes.', Sydney, Australia (2019)
|2019||Rowe C, Boelaert K, Colley S, Ballard M, Pracey P, Giblet N, Sharma N, 'Integrated thyroid nodule risk stratification using BTA U (ultrasound) and Thy (cytology): outcomes at a large tertiary centre.', Sydney, Australia (2019)|
Rowe C, Tolosa Gonzalez JT, Faulkner S, Paul JW, Gedye C, McGrath S, et al., 'The precursor for nerve growth factor (proNGF) is detectable in the rinse of fine needle aspiration biopsy of thyroid cancer', Boston, Massachussetts (2017)
|Show 21 more conferences|
Grants and Funding
|Number of grants||5|
Click on a grant title below to expand the full details for that specific grant.
20181 grants / $397,528
Hunter Cancer Biobank$397,528
Funding body: NSW Health Pathology - Pathology North
|Funding body||NSW Health Pathology - Pathology North|
|Project Team||Professor Marjorie Walker, Laureate Professor Rodney Scott, Conjoint Professor Stephen Ackland, Mrs Susan Goode, Associate Professor Pradeep Tanwar, Associate Professor Nikki Verrills, Professor Hubert Hondermarck, Doctor Simon King, Mr Ricardo Vilain, Associate Professor Nikola Bowden, Doctor Kelly Kiejda, Associate Professor Simon Keely, Doctor Christopher Rowe|
|Type Of Funding||C2220 - Aust StateTerritoryLocal - Other|
20171 grants / $15,000
Funding body: Hunter Cancer Research Alliance (HCRA)
|Funding body||Hunter Cancer Research Alliance (HCRA)|
Christopher Rowe, Hubert Hondermarck, Roger Smith, Shaun McGrath, Simon King, Marjorie Walker, John Attia
|Scheme||HCRA Implementation Flagship program|
|Type Of Funding||Grant - Aust Non Government|
20162 grants / $40,000
Funding body: AVANT Mutual Group
|Funding body||AVANT Mutual Group|
Christopher Rowe, Jonathan Paul, Jorge Tolosa, Roger Smith
|Scheme||Doctors in Training Scholarship Scheme|
|Type Of Funding||Grant - Aust Non Government|
Funding body: Hunter New England Health
|Funding body||Hunter New England Health|
|Scheme||Clinical Research Fellowship|
|Type Of Funding||Other Public Sector - State|
20151 grants / $20,000
Funding body: John Hunter Charitable Trust
|Funding body||John Hunter Charitable Trust|
Christopher Rowe, Shamasunder Acharya, Lin Perry, Katie Wynne
|Scheme||John Hunter Charitable Trust Grant|
|Type Of Funding||Other Public Sector - State|