A pragmatic digital health informatics based approach for aiding clinical prioritisation and reducing backlog of care: A study in cohort of 4022 people with diabetes.

BACKGROUND AND AIMS: The backlog of care in resource stretched healthcare systems requires innovative approaches to aid clinical prioritisation. Our aim was to develop an informatics tool to identify and prioritise people with diabetes who are likely to deteriorate whilst awaiting an appointment to optimise clinical outcomes and resources. MATERIALS AND METHODS: Using data from electronic health care records we identified 6 risk-factors that could be addressed in 4022 people (52% male, 30% non-Caucasian) with diabetes attending a large university hospital in London. The risk-factors were new clinical events/data occurring since their last routine clinic visit. To validate and compare data-led prioritisation tool to a traditional 'clinical approach' a sample of 450 patients were evaluated. RESULTS: Of the 4022 people, 549 (13.6%) were identified as having one or more risk events/factors. People with risk were more likely to be non-Caucasian and had greater socio-economic deprivation. Taking clinical prioritisation as the gold standard, informatics tool identified high risk patients with a sensitivity of 83% and lower risk patients with a specificity of 81%. An operational pilot pathway over 3 months using this approach demonstrated in 101 high risk people that 40% received interventions/care optimisation to prevent deterioration in health. CONCLUSION: A pragmatic data-driven method identifies people with diabetes at highest need for clinical prioritisation within restricted resources. Health informatics systems such as our can enhance care and improve operational efficiency and better healthcare delivery for people with diabetes.

Frailty Is Associated with Impaired Diabetic Foot Ulcer Healing and All-Cause Re-Hospitalization.

BACKGROUND: Diabetic Foot Ulcers (DFUs) are a common and feared complication of type 1 and type 2 diabetes. People with DFUs often present a significant clinical complexity due to multimorbidity, frailty, polypharmacy, and disabling conditions. Frailty, defined using the accumulation of health deficits model, has shown to predict worsening health status, hospitalizations, and death in older persons. There are no clinical studies, to date, that have examined the prevalence and effect of frailty on DFUs outcomes. The aim of our study was to explore the impact of frailty on DFUs healing and re-hospitalization in a cohort of patients hospitalized with DFUs. DESIGN: prospective cohort study. SETTING AND PARTICIPANTS: The frailty status of 76 consecutive hospitalized patients with DFUs was assessed by using the Frailty Index (FI). MEASUREMENTS: The primary outcome was the non-healing of the DFU. Secondary outcome was re-hospitalization events (for any cause) within 6 months from hospital discharge. Frailty was defined as FI>0.25. RESULTS: Out of 76 patients (median age 65 years, range 31-84), 56 (74%) were frail. At six months, 81.5% of frail patients had non-healing of the DFU compared to 55% in non-frail patients (p=0.02). The rate of of re-hospitalization was also higher in frail compared to non-frail (90.3% vs 54%, respectively; p=0.01) patients. In multivariable analyses, frailty was significantly associated with a more than fivefold increased risk of DFU non-healing [odds ratio 5.54 (95% confidence interval 1.28-23.91), p=0.02]. Similarly, re-hospitalization was also significantly higher in frail patients compared to the non-frail ones. CONCLUSIONS: In hospitalized patients with DFUs, frailty was highly prevalent. Frailty emerged as an independent risk factor for DFU non-healing and re-hospitalization events. Patients with DFUs require a comprehensive assessment of their frailty status which would enable personalization of their management and interventions.

Management of hypertension and renin-angiotensin-aldosterone system blockade in adults with diabetic kidney disease: Association of British Clinical Diabetologists and the Renal Association UK guideline update 2021.

People with type 1 and type 2 diabetes are at risk of developing progressive chronic kidney disease (CKD) and end-stage kidney failure. Hypertension is a major, reversible risk factor in people with diabetes for development of albuminuria, impaired kidney function, end-stage kidney disease and cardiovascular disease. Blood pressure control has been shown to be beneficial in people with diabetes in slowing progression of kidney disease and reducing cardiovascular events. However, randomised controlled trial evidence differs in type 1 and type 2 diabetes and different stages of CKD in terms of target blood pressure. Activation of the renin-angiotensin-aldosterone system (RAAS) is an important mechanism for the development and progression of CKD and cardiovascular disease. Randomised trials demonstrate that RAAS blockade is effective in preventing/ slowing progression of CKD and reducing cardiovascular events in people with type 1 and type 2 diabetes, albeit differently according to the stage of CKD. Emerging therapy with sodium glucose cotransporter-2 (SGLT-2) inhibitors, non-steroidal selective mineralocorticoid antagonists and endothelin-A receptor antagonists have been shown in randomised trials to lower blood pressure and further reduce the risk of progression of CKD and cardiovascular disease in people with type 2 diabetes. This guideline reviews the current evidence and makes recommendations about blood pressure control and the use of RAAS-blocking agents in different stages of CKD in people with both type 1 and type 2 diabetes.

Elevated obstructive sleep apnoea risk score is associated with poor healing of diabetic foot ulcers: a prospective cohort study.

AIMS: To assess the prevalence of risk factors for obstructive sleep apnoea in people with diabetic foot ulcers and to determine whether this risk predicts diabetic foot ulcer healing. METHODS: We studied 94 consecutive people (69% men) with diabetic foot ulcers (Type 2 diabetes, n=66, Type 1 diabetes, n=28) attending a university hospital foot unit. All participants were screened for obstructive sleep apnoea using the STOP-BANG questionnaire, with a score ≥4 identifying high risk of obstructive sleep apnoea. The primary outcome was poor diabetic foot ulcer healing, defined as diabetic foot ulcer recurrence (diabetic foot ulcers which healed and re-ulcerated in same anatomical position) and/or diabetic foot ulcer persistence (no evidence of healing on clinical examination). All participants were evaluated at 12 months. RESULTS: Of the 94 participants, 60 (64%) had a STOP-BANG score ≥4. Over 12 months, 27 participants with a score ≥4 had poor diabetic foot ulcer healing as compared to seven with a score <4 (45% vs 20.5%; P=0.025). A STOP-BANG score ≥4 significantly increased the relative risk of poor healing more than twofold, independently of other risk factors in multivariable analyses. CONCLUSIONS: There is a high prevalence of features and risk of obstructive sleep apnoea in people with diabetic foot ulcers. A STOP-BANG score ≥4 predicts poor diabetic foot ulcer healing. Obstructive sleep apnoea may be a potential, modifiable risk factor/treatment target to improve diabetic foot ulcer outcomes.

Successful management of refractory diabetic gastroparesis with long-term Aprepitant treatment.

BACKGROUND: People with gastroparesis who develop treatment-resistant (refractory) disease pose a difficult challenge, especially in the setting of end-stage renal disease (ESRD) or post pancreas transplant. Aprepitant (a neurokinin-receptor antagonist) is licensed for the short-term treatment of chemotherapy-induced nausea. There is lack of information on its long-term efficacy and safety in people with diabetic gastroparesis. CASE REPORT: Case 1 was 73-year-old man with Type 2 diabetes of 25 years' duration and ESRD requiring dialysis. He was referred to our unit as his severe symptoms of gastroparesis had failed to respond to multiple medications and resulted in frequent hospital admissions. Aprepitant, which can be used in ESRD, resulted in significant improvement in his symptoms of nausea and vomiting within weeks, and he remained on this long term (18 months) with continued benefits and had no further gastroparesis-related hospital admissions. Case 2 was a 44-year-old man with Type 1 diabetes of 41 years' duration with a history of severe hypoglycaemic events that required a pancreas transplant. Despite normoglycaemia, his symptoms of gastroparesis persisted and failed to respond to multiple medications and frequent botulinum toxin injections. He was commenced on aprepitant with significant improvement in symptoms and has remained on treatment for 12 months with sustained benefits. CONCLUSION: We describe two cases in which long-term aprepitant treatment proved effective in alleviating severe symptoms of gastroparesis that had failed to respond to conventional first-line medical treatments. Our cases highlight the need for novel treatments for managing refractory diabetic gastroparesis.

Improvements in stage of change correlate to changes in dietary intake and clinical outcomes in a 5-year lifestyle intervention in young high-risk Sri Lankans.

The objectives of a stage-matched approach to lifestyle change are that individuals progress forward through the stages of change. It also posits that progression through the stages of change is associated with positive changes in lifestyle behaviours. Measuring the relationship between stage of change and food intake is challenging due to the plurality of dietary behaviours. Furthermore, it is not clear whether changes in behaviour are sustained long-term. In this study we assess the movement through stages of change in the intensive (visits every 3months) and control groups (visits annually) of a large-scale primary prevention study in cardiovascular disease, carried out in 2637 children and young adults in Sri Lanka between 2007 and 2012. We also examine their relationship to dietary behaviours and clinical outcomes. We demonstrate that individuals in both groups continue to progress through stages of change over the course of the study and that measures of dietary behaviours improved from baseline to final follow-up. We also demonstrate that stage of change positively correlates to dietary behaviours including the ratio of recommended:not-recommended items, unpolished:polished starches and low-fat:high-fat food items throughout each year of the study. Finally, participants in the later stages of change at Y2, Y3 and Y4, had a significantly attenuated increase in weight and waist circumference at the final visit in both groups. We therefore demonstrate the usefulness of stage-matched approach in modifying complex dietary behaviours, and that stage of change is a valid measure of dietary behaviours across a large population over time.

Painful foot drop; a presentation of diabetic muscle infarction.

BACKGROUND: Macro- and microvascular complications of diabetes are varied and can present with a range of clinical signs and symptoms. Diabetic muscle infarction is a rare vascular complication of diabetes that is often not recognized. CASE REPORT: We report a case of diabetic muscle infarction, where a 65-year-old woman with Type 2 diabetes presented with acute-onset severe pain in her right leg and foot drop. CONCLUSIONS: Her foot drop was a result of a concomitant compression nerve injury as a consequence of the muscle oedema following infarction. Our case highlights the importance of early recognition and investigation of atypical presentations of vascular complications of diabetes.

Evidence for renoprotection by blockade of the renin-angiotensin-aldosterone system in hypertension and diabetes.

The incidence of end-stage renal disease (ESRD) is rising worldwide, accompanied by corresponding increases in the risk of morbidity and mortality. Underlying this trend are increasing rates of hypertension and diabetes mellitus, the two most common causes of ESRD. In addition to the adverse haemodynamic effects of hypertension on the kidney, elevated blood pressure (BP) can activate components of the renin-angiotensin-aldosterone system (RAAS), which, in turn, activate mediators of inflammation, oxidative stress, cell growth, and matrix accumulation. Lowering BP reduces the risk of cardiovascular events and renal damage. Accumulating evidence from clinical and laboratory studies suggests that interrupting the RAAS with therapies such as angiotensin-converting enzyme inhibitors, angiotensin II receptor blockers, and aldosterone receptor blockers can interfere with the mechanisms that promote diabetic and non-diabetic renal damage. Moreover, clinical trials of RAAS blockade have demonstrated reductions in microalbuminuria, a predictor of increased cardiorenal risk and overt nephropathy in patients with and without diabetes and/or hypertension. In this way, agents that block the RAAS should be considered the drugs of first choice as they provide enhanced renoprotection compared with other classes of antihypertensive agents such as calcium channel blockers and beta-blockers.

Direct regulation of insulin secretion by angiotensin II in human islets of Langerhans.

AIMS/HYPOTHESIS: This study aimed to identify the expression of angiotensin II receptors in isolated human islets and beta cells and to examine the functional consequences of their activation. MATERIALS AND METHODS: Single-cell RT-PCR was used to identify whether human islet cells express mRNA for type 1 angiotensin II receptors (AT(1)), and western blotting was used to determine AT(1) protein expression by human islets and MIN6 beta cells. We measured changes in intracellular calcium by microfluorimetry using Fura 2-loaded MIN6 cells and human islet cells. Dynamic insulin secretory responses were determined by RIA following perifusion of human islets and MIN6 cells. RESULTS: Human islets expressed mRNAs for both the angiotensin precursor, angiotensinogen, and for angiotensin-converting enzyme. In addition, human and mouse beta cells expressed AT(1). These were functionally coupled to increases in intracellular calcium, which occurred at least in part through phospholipase-C-sensitive mechanisms and calcium influx through voltage-operated calcium channels. Short-term exposure of human islets and MIN6 cells to angiotensin II caused a rapid, short-lived initiation of insulin secretion at 2 mmol/l glucose and potentiation of insulin secretion induced by glucose (at 8 and 16.7 mmol/l). CONCLUSIONS/INTERPRETATION: These data demonstrate that the AT(1) is expressed by beta cells and that angiotensin II effects a short-lived and direct stimulation of human and mouse beta cells to promote insulin secretion, most probably through elevations in intracellular calcium. Locally produced angiotensin II may be important in regulating a coordinated insulin secretory response from beta cells.