Iron-induced hypophosphataemic osteomalacia remains under-recognized as a potential complication of parenteral iron therapy. We here report two cases of symptomatic hypophosphataemic osteomalacia with multiple insufficiency fractures in the context of chronic gastrointestinal blood loss, necessitating monthly iron polymaltose infusions over prolonged periods of time. Respective blood tests revealed severe hypophosphataemia [0.29 and 0.43; normal range (NR) 0.8-1.5 mmol/l] in the presence of normal serum calcium and 25-hydroxy vitamin D levels. Urinary fractional phosphate excretion was elevated (16% and 24%; NR < 5%) and the tubular maximum phosphate reabsorption was reduced, consistent with renal phosphate wasting. Serum fibroblast growth factor 23 (FGF23) obtained in one patient was significantly elevated at 285 pg/ml (NR < 54 pg/ml). Bone mineral density was significantly reduced and whole-body bone scans revealed metabolic bone disease and multiple insufficiency fractures consistent with osteomalacia. Cessation of iron infusions resulted in clinical and biochemical improvement within 2 months in one patient whereas the second patient required phosphate and calcitriol supplementation to improve symptomatically. Iron-induced hypophosphataemic osteomalacia is thought to be due to reduced degradation of FGF23, resulting in phosphaturia and reduced synthesis of 1,25-dihydroxy vitamin D. Monitoring of patients on long-term parenteral iron is recommended to avoid clinically serious adverse effects.
We aimed to describe the current state of specialist obesity services for adults with clinically severe obesity in public hospitals in Australia, and to analyse the gap in resources based on expert consensus. We conducted two surveys to collect information about current and required specialist obesity services and resources using open-ended questionnaires. Organizational level data were sought from clinician expert representatives of specialist obesity services across Australia in 2017. Fifteen of 16 representatives of current services in New South Wales (n = 8), Queensland (n = 1), Victoria (n = 2), South Australia (n = 3), and the Australian Capital Territory (n = 1) provided data. The composition of services varied substantially between hospitals, and patient access to services and effective treatments were limited by strict entry criteria (e.g. body mass index 40 kg/m or higher with specific complication/s), prolonged wait times, geographical location (major cities only) and out-of-pocket costs. Of these services, 47% had a multidisciplinary team (MDT), 53% had an exercise physiologist/physiotherapist, 53% had a bariatric surgeon and 33% had pharmacotherapy resources. Key gaps included staffing components of the MDT (psychologist, exercise physiologist/physiotherapist) and access to publicly funded weight loss pharmacotherapy and bariatric surgery. There was consensus on the need for significant improvements in staff, physical infrastructure, access to services, education/training in obesity medicine and targeted research funding. Based on the small number of existing, often under-resourced specialist obesity services that are located only in a few major cities, the vast majority of Australians with clinically severe obesity cannot access the specialist evidence based treatments needed.
Introduction. Obesity and diabetes are difficult to treat in public clinics. We sought to determine the effectiveness of the Metabolic Rehabilitation Program (MRP) in achieving long-term weight loss and improving glycaemic control versus “best practice” diabetes clinic (DC) in obese patients using a retrospective cohort study. Methods. Patients with diabetes and BMI > 30 kg/m2 who attended the MRP, which consisted of supervised exercise and intense allied health integration, or the DC were selected. Primary outcomes were improvements in weight and glycaemia with secondary outcomes of improvements in blood pressure and lipid profile at 12 and 30 months. Results. Baseline characteristics of both cohorts (40 MRP and 40 DC patients) were similar at baseline other than age (63 in MRP versus 68 years in DC, P = 0.002). At 12 months, MRP patients lost 7.65 ± 1.74 kg versus 1.76 ± 2.60 kg in the DC group (P < 0.0001) and 9.70 ± 2.13 kg versus 0.98 ± 2.65 kg at 30 months (P < 0.0001). Similarly, MRP patients had significant absolute reductions in %HbA1c at 30 months versus the DC group (−0.86 ± 0.31% versus 0.12% ± 0.33%, P < 0.038), with nonsignificant improvements in lipids and blood pressure in MRP patients. Conclusion. Further research is needed to establish the MRP as an effective strategy for achieving sustained weight loss and improving glycaemic control in obese patients with type 2 diabetes.
Purpose Type 2 diabetes mellitus has become a major concern of Australian healthcare providers. From rates of barely more than 1 percent in the mid-90s, diabetes is now the leading cause of morbidity in the country. To combat the growing diabetes epidemic, Western Sydney Local Health District created the Western Sydney Diabetes (WSD) initiative. One of the key components of the WSD initiative since 2014 has been joint specialist case conferencing (JSCC). The purpose of this paper is to evaluate the JSCC service including both individual- and practice-based changes. Design/methodology/approach The authors evaluated the JSCC program by conducting an analysis of patient-level data in addition to a discrete practice-level study. The study aim was to examine both the effect on individual patients and the practice, as well as acceptability of the program for both doctors and their patients. The evaluation included data collection and analysis of primary patient outcomes, as well as a survey of GPs and patients. Patient data on primary outcomes were obtained by accessing and downloading them through GP practice management software by GP practice staff. Findings The authors found significant improvements at both the patient levels, with reductions in BMI, HbA1c and blood pressure sustained at three years, and at the practice level with improvements in markers of patient management. The authors also found high acceptability of the program from both patients and GPs. Originality/value This paper provides good evidence for the use of a JSCC program to improve diabetes management in primary care through capacity building with GPs.
We report a 72-year-old female patient with diffuse large B cell non-Hodgkin's lymphoma (NHL) with previous treatment with standard chemotherapy presenting as an acute, ascending, sensorimotor polyneuropathy. Nerve conduction studies and lumbar puncture supported a rare, but ominous, axonal variant of Guillain-Barré Syndrome (GBS) known as acute motor and sensory axonal neuropathy (AMSAN), which is distinguished from the more common, acute demyelinating forms of GBS. Previous reports have largely focused on toxicities secondary to chemo- or radiotherapy as a major contributor to the development of acute neuropathies in malignancy. Clinicians should also be mindful of direct neoplastic invasion or, less commonly, paraneoplastic phenomenon, as alternative mechanisms, the latter possibly reflecting immune dysregulation in particularly aggressive lymphomas. At the time of writing, this is the first report in the literature of an axonal variant of GBS in a patient with diffuse large B cell NHL. A discussion regarding common and uncommon neuropathies in haematological malignancies is made, with a brief review of the anecdotal evidence supporting a paraneoplastic association with GBS or its variant forms in the setting of lymphoma.
Context The etiological mechanism of bile acid (BA) effects on insulin resistance and obesity is unknown. Objective This work aimed to determine whether plasma BAs are elevated in human obesity and/or insulin resistance. Methods This observational study was conducted at an academic research center. Seventy-one adult volunteers formed 4 groups: lean insulin-sensitive (body mass index [BMI] ≤ 25 kg/m2, Homeostatic Model Assessment of Insulin Resistance [HOMA-IR] < 2.0, n = 19), overweight/obese nondiabetic who were either insulin sensitive (Obsensitive, BMI > 25 kg/m2, HOMA-IR < 1.5, n = 11) or insulin resistant (Obresistant, BMI > 25 kg/m2, HOMA-IR > 3.0, n = 20), and type 2 diabetes (T2D, n = 21). Main outcome measures included insulin sensitivity by hyperinsulinemic-euglycemic clamp, body composition by dual energy x-ray absorptiometry, abdominal fat distribution, and liver density by computed tomography and plasma BA. Results In the Obresistant group, glucose infusion rate/fat-free mass (GIR/FFM, an inverse measure of insulin resistance) was significantly lower, and visceral and liver fat higher, compared to lean and Obsensitive individuals, despite similar total adiposity in Obresistant and Obsensitive. Total BA concentrations were higher in Obresistant (2.62 ± 0.333 mmol/L, P = .03) and T2D (3.36 ± 0.582 mmol/L, P < .001) vs Obsensitive (1.16 ± 0.143 mmol/L), but were similar between Obsensitive and lean (2.31 ± 0.329 mmol/L) individuals. Total BAs were positively associated with waist circumference (R = 0.245, P = .041), visceral fat (R = 0.360, P = .002), and fibroblast growth factor 21 (R = 0.341, P = .004) and negatively associated with insulin sensitivity (R = –0.395, P = .001), abdominal subcutaneous fat (R = –0.352, P = .003), adiponectin (R = –0.375, P = .001), and liver fat (Hounsfield units, an inverse marker of liver fat, R = –0.245, P = .04). Conjugated BAs were additionally elevated in T2D individuals (P < .001). Conclusions BA concentrations correlated with abdominal, visceral, and liver fat in humans, though an etiological role in insulin resistance remains to be verified.
Background. Artifactual hypoglycaemia, defined as a discrepancy between glucometer (capillary) and plasma glucose levels, may lead to overtreatment and costly investigations. It is not infrequently observed in patients with Raynaud's phenomenon due to vascular capillary distortion, yet this is clinically underappreciated. Case Report. We report a 76-year-old woman with systemic sclerosis and Raynaud's phenomenon, who presented with upper gastrointestinal bleeding and found to have concomitant persistent hypoglycaemia (1.0–2.7mmol/L) on a point-of-care glucometer in the absence hypoglycaemic symptoms. She underwent a 2-week hospital admission, repeated glucose monitoring, hydrocortisone replacement and dextrose infusions, with consequent hyperglycaemia on plasma measurements. Clinically, she did not satisfy Whipple's triad and radiological investigations failed to identify pituitary or pancreatic pathology. A 72-hour fast was negative for hyperinsulinaemia or exogenous insulin use and her sulphonylurea metabolite urinary screen was negative. Discussion. Treatment of low capillary blood glucose is usually met with clinical impetus to treat, even when hypoglycaemic symptoms are lacking. The correct diagnosis may have been achieved had there been an observation of her cold hands, scleroderma facies, and consideration of the likely distorted peripheral microvasculature. Early identification of this presumably rare clinical scenario may have prevented overtreatment, altered methods of monitoring, and avoided unnecessary investigations.
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