ORCID Profile
0000-0001-8643-1773
Current Organisation
University of Adelaide
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Publisher: BMJ
Date: 12-2020
DOI: 10.1136/BMJDRC-2020-001837
Abstract: In people accepted onto a bariatric surgery program we compared diabetes-related outcomes in those who completed surgery with those who withdrew before having surgery—examining rates of insulin use in people with type 2 diabetes (T2D), and rates of incident diabetes in people without pre-existing T2D. 771 people were accepted onto the program. 463 people (60%) had T2D at referral, of which 48% completed surgery and 52% withdrew. Of 308 people without T2D at referral, 49% completed surgery, and 51% withdrew. Rates of insulin use and incident diabetes were compared by Kaplan-Meier analyses. Among those with pre-existing T2D, we examined rates of remission and relapse after surgery. People without T2D who withdrew from the program had higher mean body mass index and glycated hemoglobin levels than those completing surgery (p .005). The rate of incident diabetes at 5 years was 19% in those who withdrew versus 0% in those completing surgery (p .001). 30% of people with T2D were taking insulin at referral and all stopped insulin after surgery. During follow-up, the rate of insulin (re)introduction was lower in those who completed surgery (8% vs 26% at 5 years, p .001). Of those with T2D who completed surgery, 80% had remission, but 34% had relapsed by 5 years. Diabetes relapse was associated with less weight loss after surgery, a longer duration of T2D and previous insulin use. Despite a high relapse rate, people with T2D who completed surgery had lower insulin use at 5 years than those withdrawing from the program. In people without T2D, bariatric surgery prevented incident diabetes. People without T2D who withdrew from the program were at greater risk of diabetes, suggesting those who could benefit the most in terms of T2D prevention are not completing bariatric surgery.
Publisher: Wiley
Date: 31-01-2023
DOI: 10.1111/LIV.15524
Publisher: Springer Science and Business Media LLC
Date: 11-07-2023
DOI: 10.1007/S11154-022-09745-6
Abstract: Adrenal insufficiency requires prompt diagnosis in pregnancy, as untreated, it can lead to serious consequences such as adrenal crisis, intrauterine growth restriction and even foetal demise. Similarities between symptoms of adrenal insufficiency and those of normal pregnancy can complicate diagnosis. Previously diagnosed adrenal insufficiency needs monitoring and, often, adjustment of adrenal hormone replacement. Many physiological changes occur to the hypothalamic-pituitary-adrenal (HPA) axis during pregnancy, often making diagnosis and management of adrenal insufficiency challenging. Pregnancy is a state of sustained physiologic hypercortisolaemia there are multiple contributing factors including high plasma concentrations of placental derived corticotropin-releasing hormone (CRH), adrenocorticotropin (ACTH) and increased adrenal responsiveness to ACTH. Despite increased circulating concentrations of CRH-binding protein (CRH-BP) and the major cortisol binding protein, corticosteroid binding globulin (CBG), free concentrations of both hormones are increased progressively in pregnancy. In addition, pregnancy leads to activation of the renin-angiotensin-aldosterone system. Most adrenocortical hormone diagnostic thresholds are not applicable or validated in pregnancy. The management of adrenal insufficiency also needs to reflect the physiologic changes of pregnancy, often requiring increased doses of glucocorticoid and at times mineralocorticoid replacement, especially in the last trimester. In this review, we describe pregnancy induced changes in adrenal function, the diagnosis and management of adrenal insufficiency in pregnancy and areas requiring further research.
Publisher: Wiley
Date: 19-02-2019
DOI: 10.1002/JBMR.3670
Abstract: Camurati-Engelmann disease (OMIM 31300) is a rare cranio-tubular bone dysplasia characterized by osteosclerosis of the long bones and skull caused by dominantly-inherited mutations in the transforming growth factor beta 1 (TGFB1) gene. A wide variation in phenotype has been recognized, even within families carrying the same mutation. In addition, aspects of the natural history of the disorder, in particular whether it is always progressive or can remit spontaneously, remain uncertain. In a large kindred carrying a TGFB1 gene mutation (c.653G > A p.R218H) we have attempted to clarify the extent of phenotypic variability and the natural history of the disease through detailed in idual histories of symptoms, and skeletal imaging by both radiography and scintigraphy. Only one subject had the classical childhood onset with bone pain in the legs and gait disturbance. Eight subjects reported the onset of leg pain in their teenage years that, by their early 20s, had either resolved or persisted at a low level. Two of these eight later developed cranial nerve palsies. There was a wide variation in the radiographic appearance in adults, but disease extent and activity in long bones, as assessed by scintigraphy, was inversely correlated with age (p < 0.025). In younger subjects the radiographic and scintigraphic appearances were concordant, but in older subjects the scintigram could be quiescent despite florid radiographic changes. Sequential scintigrams in two subjects showed reduced activity in the later scan. One subject had suffered meningoencephalitis in early childhood that resulted in paresis of one arm. The affected arm showed markedly less disease involvement, implicating mechanical or growth factors in its etiology. Our data suggest that the natural history of Camurati-Engelmann disease can be benign, and that disease activity commonly attenuates in adulthood. Severe cases of childhood onset and/or with cranial nerve involvement, may occur only in a minority of mutation carriers. © 2019 American Society for Bone and Mineral Research.
No related grants have been discovered for Jessica Lee.