The ankle-brachial index (ABI) is a fast, simple, noninvasive method that provides accurate results in the early diagnosis of peripheral artery disease. Microalbuminuria is considered a predictor of renal and cardiovascular complications in patients with diabetes. This study was conducted to determine the correlation between ABI and microalbuminuria with certain risk factors in patients with type 2 diabetes.
Subjects and research methods: A cross-sectional descriptive study was performed on 62 inpatients with type 2 diabetes. All patients were measured for ABI as well as microalbuminuria, HbA1c, glucose and lipidemia in the blood.
Results: The study results showed that in patients with dyslipidemia, the risk of having microalbuminuria (+) increased 5.7 times and ABI ≤0.90 increased 8.6 times (P = 0.004 and 0.021, respectively). Fasting blood glucose >7.2 mmol/L had 5.7 times higher microalbuminuria (+) risk and 8.6 times higher ABI ≤0.90 (P = 0.004 and 0.021, respectively). Patients with HbA1c ≥7% were 2.9 times more likely to have microalbuminuria (+) and ABI ≤0.90 (P = 0.043 and 0.048, respectively).
Conclusions: Peripheral vascular disease risk factors such as hypertension, dyslipidemia and waist circumference and the effectiveness of fasting blood glucose and HbA1c control increased the risk of high microalbuminuria and ABI in patients with type 2 diabetes.
Background: The short synacthen test (SST) is the most commonly performed investigation to assess adrenal function. Appropriate criteria for when an SST is performed are subject to debate. We investigated how random serum cortisol levels relate to SST response.
Methods: We examined random cortisol measurements taken between 04.40-23.55 p.m. results of SST baseline and 30-/60-min cortisol performed over 12 months (225 SSTs) at Salford Royal Hospital. Serum cortisol was measured on the Siemens Centaur Analyser.A 30-60-min cortisol concentration of ≥450 nmol/L defined a pass; 350-449 nmol/L defined borderline.
Results: Patients only proceeded to SST if random cortisol was <400 nmol/L. For those not on corticosteroids for at least 2 weeks, 42/43 (97.7%) cases with random cortisol concentration of ≥200 nmol/L had an SST 'pass'. The relation was less clear with corticosteroid treatment (19/35 cases; 54%).For those not taking glucocorticoid treatment (including inhaled/topical corticosteroids) in the previous 2 weeks, 91.8% of SSTs were pass/2.7% borderline/5.5% fail. For those on steroids, 51.9% of SSTs were a pass/11.4% were borderline.In relation to the postsynacthen cortisol pass cut-off of ≥450 nmol/L, in 15/207 (7.2%) of cases, the 60-min cortisol was ≥450 nmol/L (adequate adrenocortical function), but 30-min cortisol was below this. In all cases where the 30-min cortisol did indicate a pass (i.e. was ≥450 nmol/L) the 60-min cortisol was also ≥450 nmol/L.
Conclusion: Our findings suggest that if the random cortisol level is ≥200 nmol/L, regardless of the time of day and the person was not taking corticosteroid treatment in the previous 2 weeks, SST may not be needed. Our data also suggests that 60-min cortisol retains utility.
Introduction: Many people with type 1 diabetes (T1DM) continue to run high HbA1c levels with an associated elevated risk of cardiovascular events and increased mortality. We describe here how adjunctive prescription of an SGLT2 inhibitor has improved the glycaemic control of several people with T1DM, where the new technology has been intensively deployed.
Methods: We report outcomes of six adults with T1DM who have been given dapagliflozin in East Cheshire, UK. Initiation was with education/support from the diabetes specialist nurses. All had an HbA1c of 70 mmol/mol (8.6%) or more before this was initiated. All had been monitoring glycemia with a FreeStyle Libre monitor for at least 6 months prior to this.
Results: The age range was 30-68 years. The mean duration of T1DM was 23.3 ± 5.5 years. All were on a basal-bolus regime. Over a 6 month period, HbA1c fell from 78.5 mmol/mol (9.3%) to 55 mmol/mol (7.2%). The greatest reduction in HbA1c was 57 mmol/mol (7.4%). Analysis of the FreeStyle Libre blood glucose records showed that the proportion of blood glucose readings on target (4-10 mmol/L) increased from 33.1 to 65.2% with the addition of dapagliflozin(P = 0.007). The proportion of blood glucose readings above target (>10 mmol/L) decreased from 68.0 to 26.4%, 6 months after initiation of dapagliflozin (P = 0.005). There was no increase in symptomatic hypoglycemia.
Conclusion: Dapagliflozin as adjunctive therapy to basal-bolus regime insulin in individuals with T1DM was well tolerated and improved glycemic control with no increase in hypoglycemia. We provide further evidence of the value of this intervention.
Management of patients with diabetes and renal transplant could be challenging. Transplant patients use multiple immune suppressants that can worsen or even trigger hyperglycemia. There are no data about the use of the new class of sodium-glucose co-transporter-2 (SGLT-2) inhibitor dapagliflozin in patients with renal transplant and diabetes.
Case series: Four patients, with diabetes, who are attending the diabetes clinic at our institution, are presented here. They were all counseled to be started on dapagliflozin 10 mg to improve diabetes control as they were on multiple agents and not achieving targets. All four patients showed significant improvement in hemoglobin A1c, with no adverse effects on renal parameters and had favorable effect on weight and blood pressure (BP).
Conclusion: Use of the SGLT-2 inhibitor dapagliflozin in the standard dose of 10 mg helped to achieve satisfactory control with favorable effects on BP and weight with no adverse effects on renal function.
Atypical hemolytic uremic syndrome (aHUS), a challenging disorder, commonly caused by inherited defects or regulatory processes of the complement alternative pathway. There are multiple causes, including pregnancy. Pregnancy provokes life-threatening episodes, preeclampsia, hemolysis elevated liver enzymes low platelets, microangiopathic hemolytic anemia (MAHA) and end-stage renal disease. Additionally, complement dysregulation and, with aHUS, affects fetal and maternal outcomes. Pregnancy-associated aHUS results in a poor prognosis with irreversible renal damage. Likewise, it is imperative to know that MAHA can provoke endothelial disruption, destruction of red cells and thrombocytopenia. We present a case of a young 18-year-old woman with MAHA and aHUS, requiring emergent cesarean section at 34 weeks of gestation and hemodialysis, secondary to complications from a recent pregnancy. Elevated blood pressure readings, rising creatinine levels, as well as her mother being on dialysis after pregnancy raised suspicion for thrombotic microangiopathy and aHUS. She was subsequently managed with plasma exchange, steroids, eculizumab and hemodialysis. Thus, plasma exchange should be initiated, with pending additional workup. Upon a definitive diagnosis of aHUS, eculizumab would be warranted to mitigate immune dysregulation. Understanding thrombotic microangiopathies diagnosis, and recognizing concomitant consequences, is vital. Having better insights into endothelial injuries can prevent unfortunate outcomes.
Sodium-glucose co-transporter 2 Inhibitors (SGLT2i) were initially developed as therapeutic options for patients with type 2 diabetes mellitus (T2DM). Recently, randomized clinical trials have investigated their effects in cardiorenal protection through major adverse cardiovascular event reduction and reductions in diabetic nephropathy. While multiple mechanisms are proposed for this protection, microvascular protection is the primary component of their efficacy. While not primarily emphasized in clinical trials, evidence in other studies suggests that SGLT2i may confer retinoprotective effects via some of the same mechanisms in the aforementioned cardiorenal trials. Diabetic patients are susceptible to vision loss with chronic hyperglycemia promoting inflammation, edema, and retinal pathological changes. Targeting these pathways via SGLT2i may represent opportunities for providers to decrease retinopathy in high-risk T2DM patients, reduce disease progression, and lower drug burden in diabetic retinopathy patients. Further comprehensive clinical trials investigating these associations are needed to establish the potential retinoprotective effects of SGLT2i.
Objective: Accurate diagnosis of polycystic ovarian syndrome (PCOS) enables clinical interventions/cardiometabolic risk factor management. Diagnosis can take over 2 years and multiple clinician contacts. We examined patterns of PCOS-associated biochemical investigations following initial consultation prior to pelvic ultrasound scan (USS).
Methods: We determined in 206 women (i) the range of different biochemical test panels used in the diagnosis of PCOS in primary/secondary care prior to USS relative to national guidance in the UK and (ii) the relation between testing patterns and time to USS to highlight potential delays introduced by inappropriate testing.
Results: In these 206 women, 47 different test combinations were requested at initial venepuncture; only 7 (3%) had the test panel suggested in UK guidance (follicle-stimulating hormone/luteinizing hormone/testosterone/sex hormone-binding globulin/prolactin). The number of tests performed prior to USS varied from one test to all seven tests. There was an inverse relation between the number of biochemistry tests requested at initial venepuncture episode and 'time to scan'. Those who had <3 tests had a significantly longer time from first request to USS (median 70 days) than those with 3-7 tests (median 40 days; P = 0.002). One venepuncture episode prior to USS was associated with shorter 'time to scan' (median 29 days) than those with 2-4 episodes (median 255 days; P < 0.001).
Conclusion: There was no identifiable pattern to biochemical investigations requested as part of the initial diagnostic evaluation in women with suspected PCOS. We recommend standardization of the initial biochemical panel of analytes for PCOS workup, with incorporation into hospital/general practice ordering software systems.
Objective: This systematic review/meta-analysis was conducted to investigate the relationship between rheumatoid arthritis and the incidence of diabetes mellitus.
Methods: A comprehensive search was conducted up to 10 March 2020 in Medline (via Ovid), Embase (via Ovid) and Web of Science core collection to identify cohort studies comparing the risk of diabetes mellitus incidence in people with rheumatoid arthritis with the general population. The I2 statistic was used to test heterogeneity. Pooled relative risks were calculated using random-effects models. Publication bias was assessed using Egger's test and Begg's test.
Results: The initial search provided 3669 articles. Of those, five journal articles/two conference abstracts comprising 1 629 854 participants were included in this study. The funnel plot showed potential publication bias, proven by Egger's test (-3.15, P < 0.01), but not Begg's test (-0.05, P = 1.00). Heterogeneity was observed in I2 test (I2 = 96%, P < 0.01). We found that rheumatoid arthritis was associated with a higher risk of diabetes mellitus incidence (pooled relative risk, 1.23; 95% confidence interval, 1.07-1.40). Exploration of potential sources of heterogeneity found significant heterogeneity in different countries/regions (P = 0.002), but heterogeneity was NS in different study designs (P = 0.30). Sensitivity analyses confirmed that the association between rheumatoid arthritis and diabetes mellitus incidence was robust.
Conclusion: Rheumatoid arthritis is associated with an increased risk of diabetes mellitus incidence. This finding supports the notion that inflammatory pathways are involved in the pathogenesis of diabetes. More intensive interventions targeting diabetes risk factors should be considered in people with rheumatoid arthritis.
Elevated fibroblast growth factor 23 (FGF23) is associated with cardiovascular events, particularly heart failure. Although FGF23 has been reported to induce cardiac hypertrophy, recent studies demonstrated that cardiac hypertrophy and myocardial infarction induce FGF23 production by cardiomyocytes. We aimed to explore whether acute cardiac overload increases cardiac and skeletal FGF23 expression and circulating FGF23 levels.
Methods: We administered 30 μL/g bodyweight of isotonic saline intraperitoneally in rats to induce acute cardiac overload. We measured serum FGF23 levels and other parameters of mineral metabolism at 2, 6, and 24 h after saline or sham injection. We also analyzed gene expression in the heart, calvarium, femur, and kidney at 2 and 24 h after injection.
Results: Acute saline injection induced cardiac overload as evidenced by a significant upregulation of brain natriuretic peptide along with a trend towards increased expression of atrial natriuretic peptide and mild hyponatremia. However, there were no changes in serum FGF23 levels or FGF23 expression in the heart, calvarium, or femur.
Conclusions: Acute cardiac overload by saline injection in rats did neither induce FGF23 expression in the heart or bone nor did it increase serum FGF23 levels. These findings suggest that more severe or long-term cardiac damage is required for induction of FGF23 expression.
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