Glucose patterns following alcohol and illicit drug use in young adults with type 1 diabetes: A flash glucose monitoring study.

INTRODUCTION: To assess the effects of alcohol and illicit drug use in young adults (age 18-35) with type 1 diabetes (T1D) on flash glucose monitor sensor glucose (SG) readings. METHODS: Twenty young adults with T1D were enrolled from a tertiary referral hospital outpatient department in Melbourne, Australia for a 6-week prospective observational study using flash glucose monitoring (FGM). Glucometrics comparing substance using days (SUEDs) to those without substance use (non-SUEDS) were analysed. The primary outcomes were the difference in mean SG values, its standard deviation and minutes/24-h period out of range (SG <3.9 mmol/L or >10.0 mmol/L) between matched SUEDs vs non-SUEDs. An interaction model with the primary effect of HbA1c on SG values was also performed. RESULTS: There were no differences in the primary outcome measures between SUEDS and non-SUEDs. However, there were differences in the regression coefficients for HbA1c and glucometrics between non-SUEDs and SUEDs for mean SG, time out of range and time with SG > 10 mmol/L. This difference was also identified between non-SUEDS and days of ≥40 g alcohol for mean SG. CONCLUSIONS: While there was no difference between glucometrics for SUEDs and non-SUEDs on primary outcomes, HbA1C was found to be a less reliable predictor of glucose patterns in the 24-h period following substance use than control days. Young adults with T1D need to monitor and respond to their glucose levels following substance use and engage in harm minimisation practices irrespective of baseline glucose control.

Continuous Glucose Monitoring Versus Self-Monitoring of Blood Glucose to Assess Glycemia in Gestational Diabetes.

Background: Gestational diabetes mellitus (GDM) management using self-monitoring blood glucose (SMBG) does not normalize pregnancy outcomes. Objective: We aimed to conduct an observational study to explore if continuous glucose monitoring (CGM) could identify elevated glucose levels not apparent in women with GDM managed using SMBG. Study Design: A 7-day masked-CGM (iPro; Medtronic) was performed within 2 weeks of GDM diagnosis, immediately post-GDM education, but before insulin commencement as determined by SMBG. CGM data regarding hyperglycemia (sensor glucose >126 mg/dL [06:00-00:00 h] and >99 mg/dL [00:00-06:00 h] for >10% of time), time with health care professionals, treatment, and pregnancy outcome were collected. Comparisons (Mann-Whitney test) were performed between subjects subsequently commenced on insulin versus those continued with diet and lifestyle measures alone. Results: Ninety women of mean (standard deviation) gestational age weeks 27(1) were studied. Those prescribed insulin (n = 34) compared with those managed with diet and lifestyle alone (n = 56) had a greater time in hyperglycemia (P = 0.0001). Of those not prescribed insulin, 35/56 (61%) breached CGM cutoffs between 00:00 and 06:00 h; 11/56 (20%) breached 6.00-00.00 h CGM cutoffs for >10% of the time; and 21/45 (47%) with optimal CGM glucose levels during the daytime spent >10% time in hyperglycemia between 00.00 and 06:00 h. In contrast, SMBG measurements exceeded the clinical targets of <120 mg/dL postdinner in 5.4% and <100 mg/dL fasting in 0% of the subjects. Conclusions: CGM provides a more comprehensive assessment of nocturnal hyperglycemia than SMBG and could improve targeting of interventions in GDM. Larger studies to better define CGM targets are required, which once established will inform studies aimed at targeting nocturnal glucose levels.

Experiences of young adults with type 1 diabetes while using alcohol and recreational drugs: An interpretative phenomenological analysis (IPA) of semi-structured interviews.

AIMS: Alcohol and recreational drug use is common in young adults with type 1 diabetes (T1DM) and may account for increased morbidity and mortality. This study explores the motivations and experiences unique to this population while using alcohol and recreational drugs. METHODS: Semi-structured interviews focusing on substance use were performed with 16 young adults aged 18-35 with T1DM who drink alcohol (at least 50 g, 5 Australian standard drinks, in a single session) and/or used recreational drugs. A qualitative interpretative phenomenological analysis (IPA) of the interview data was performed by three clinicians with differing expertise (a psychologist, endocrinologist and addiction medicine specialist). RESULTS: A range of motivations, experiences and harm reduction strategies regarding substance use were described specific to young adults with T1DM with most aimed at mitigating the risk of hypoglycaemia. Clinicians remained the most trusted resources, however, substance use was rarely discussed at clinical encounters. Currently available information, especially for illicit drugs, was described as inadequate. CONCLUSIONS: This analysis identified experiences unique to young adults with T1DM when using alcohol and other drugs. Understanding these experiences and how these young adults attempt to mitigate the risks of substance use may lead to improved clinical interactions and management strategies.

Alcohol and recreational drug use in young adults with type 1 diabetes.

Alcohol and other recreational drug use reaches peak prevalence in young adulthood, including for those with chronic medical conditions such as type 1 diabetes. This review summarises the current literature on the patterns of substance use amongst young adults with type 1 diabetes and the mechanisms through which alcohol and recreational drugs may affect diabetes related health outcomes. These include the direct physical effect of intoxication, as well as the effects of alcohol and drugs on mental health and glucose metabolism. Evidence for increased associated mortality and morbidity is also presented, and current guidelines, management strategies and directions for further research are discussed.

A Prospective Study of Renal Transplant Recipients: A Fall in Insulin Secretion Underpins Dysglycemia After Renal Transplantation.

BACKGROUND: Dysglycemia (encompassing impaired glucose tolerance and diabetes mellitus) arising after renal transplantation is common and confers a significant cardiovascular mortality risk. Nonetheless, the pathophysiology of posttransplant dysglycemia is not well described. The aim of this study was to prospectively and comprehensively assess glucose handling in renal transplant recipients from before to 12 months after transplantation to determine the underpinning pathophysiology. MATERIALS AND METHODS: Intravenous and oral glucose tolerance testing was conducted before and at 3 and 12 months posttransplantation. An intravenous glucose tolerance test was also performed on day 7 posttransplantation. We followed up 16 transplant recipients for 3 months and 14 recipients for 12 months. Insulin secretion, resistance and a disposition index (DI (IV)), a measure of ß cell responsiveness in the context of prevailing insulin resistance, were also determined. RESULTS: At 12 months, 50% of renal transplant recipients had dysglycemia. Dysglycemia was associated with a dramatic fall in DI (IV) and this loss in ß cell function was evident as early as 3 months posttransplantation (23.5 pretransplant; 6.4 at 3 months and 12.2 at 12 months posttransplant). Differences in the ß cell response to oral glucose challenge were evident pretransplant in those destined to develop dysglycemia posttransplant (2-hour blood glucose level 5.6 mmol/L versus 6.8 mmol/L; P < 0.01). CONCLUSIONS: Dysglycemia after renal transplantation is common, and the loss of insulin secretion is a major contributor. Subclinical differences in glucose handling are evident pretransplant in those destined to develop dysglycemia potentially heralding a susceptible ß cell which under the stressors associated with transplantation fails.

Prolonged life-threatening hypoglycaemia following dose escalation of octreotide LAR in a patient with malignant polysecreting pancreatic neuroendocrine tumour.

UNLABELLED: This paper details the case of a 77-year-old male with refractory hypoglycaemia due to inoperable metastatic pancreatic neuroendocrine tumour (pNET) co-secreting insulin and gastrin. Multiple medical therapies were trialled with limited success, and we describe the complications experienced by our patient. Somatostatin analogues can ameliorate hypoglycaemia and may have tumour-stabilising effects; however, in our case resulted in paradoxical worsening of hypoglycaemia. This rendered our patient hospital dependent for glycaemic support including continuous dextrose infusion. Although this is a reported adverse effect with initiation of therapy, we describe successful initiation of short-acting octreotide as an inpatient followed by commencement of long-acting octreotide. Hypoglycaemic collapse occurred only after dose titration of long-acting octreotide. We outline the pitfalls of somatostatin analogue therapy and the mechanisms that may contribute to worsening hypoglycaemia. This rare side effect cannot be reliably predicted, necessitating close supervision and glucose monitoring during therapy. Our patient achieved disease stabilisation and gradual resolution of hypoglycaemia with peptide receptor radionuclide therapy (PRRT), an emerging therapeutic option for metastatic neuroendocrine tumours with high efficacy and low toxicity. We present a brief but comprehensive discussion of currently available and novel therapies for insulin secreting pNETs. LEARNING POINTS: Hypoglycaemia due to malignant insulin secreting pNET is frequently severe and may be life-threatening despite supportive therapies.Octreotide can ameliorate hypoglycaemia, and may have anti-proliferative and tumour-stabilising effects in malignant pNETs that are surgically unresectable.Paradoxical worsening of hypoglycaemia may occur with octreotide initiation and dose titration, necessitating close supervision and glucose monitoring.PRRT is emerging as a therapeutic option with high efficacy and low toxicity.

Spectrum of renal disease in diabetes.

The spectrum of renal disease in patients with diabetes encompasses both diabetic kidney disease (including albuminuric and non-albuminuric phenotypes) and non-diabetic kidney disease. Diabetic kidney disease can manifest as varying degrees of renal insufficiency and albuminuria, with heterogeneity in histology reported on renal biopsy. For patients with diabetes and proteinuria, the finding of non-diabetic kidney disease alone or superimposed on the changes of diabetic nephropathy is increasingly reported. It is important to identify non-diabetic kidney disease as some forms are treatable, sometimes leading to remission. Clinical indications for a heightened suspicion of non-diabetic kidney disease and hence consideration for renal biopsy in patients with diabetes and nephropathy include absence of diabetic retinopathy, short duration of diabetes, atypical chronology, presence of haematuria or other systemic disease, and the nephrotic syndrome.

Serum sickness following rabbit anti-thymocyte globulin for acute vascular renal allograft rejection.

A simultaneous pancreas-kidney transplant recipient developed serum sickness manifesting with severe upper limb allodynia, arthralgia and myalgia 17 days following rabbit anti-thymocyte globulin (rATG) infusion for biopsy-proven vascular rejection. Rapid resolution of symptoms followed treatment with high-dose glucocorticoids. rATG is increasingly favoured over equine ATG in solid-organ transplantation, and although rATG has a superior safety profile, it is important to maintain a high index of suspicion for serum sickness.

Type 1 diabetes and latent autoimmune diabetes in adults.

The review is aimed to explore the clinical and pathogenic spectrum of autoimmune diabetes including Type 1 diabetes and latent autoimmune diabetes in adults (LADA). Genetic susceptibility modifies age at onset in autoimmune diabetes. The most important genetic susceptibility to Type 1 diabetes and LADA is in the HLA region. Because of the age-related genetic factors, LADA can not be distinguished from classic Type 1 diabetes by genetics. Non-genetic factors contribute much to Type 1 diabetes, but little is known in LADA. Diabetes-associated immune process can occur in early childhood and can be predictive of an ongoing beta cell destruction. The management and prevention of LADA need to be investigated in order to define the best therapeutic strategy.