Lower extremity arterial disease in patients with diabetes: a contemporary narrative review.

Lower-extremity arterial disease (LEAD) is a major endemic disease with an alarming increased prevalence worldwide. It is a common and severe condition with excess risk of major cardiovascular events and death. It also leads to a high rate of lower-limb adverse events and non-traumatic amputation. The American Diabetes Association recommends a widespread medical history and clinical examination to screen for LEAD. The ankle brachial index (ABI) is the first non-invasive tool recommended to diagnose LEAD although its variable performance in patients with diabetes. The performance of ABI is particularly affected by the presence of peripheral neuropathy, medial arterial calcification, and incompressible arteries. There is no strong evidence today to support an alternative test for LEAD diagnosis in these conditions. The management of LEAD requires a strict control of cardiovascular risk factors including diabetes, hypertension, and dyslipidaemia. The benefit of intensive versus standard glucose control on the risk of LEAD has not been clearly established. Antihypertensive, lipid-lowering, and antiplatelet agents are obviously worthfull to reduce major cardiovascular adverse events, but few randomised controlled trials (RCTs) have evaluated the benefits of these treatments in terms of LEAD and its related adverse events. Smoking cessation, physical activity, supervised walking rehabilitation and healthy diet are also crucial in LEAD management. Several advances have been achieved in endovascular and surgical revascularization procedures, with obvious improvement in LEAD management. The revascularization strategy should take into account several factors including anatomical localizations of lesions, medical history of each patients and operator experience. Further studies, especially RCTs, are needed to evaluate the interest of different therapeutic strategies on the occurrence and progression of LEAD and its related adverse events in patients with diabetes.

Euglycemic ketoacidosis induced by therapeutic fasting in a non-diabetic patient.

BACKGROUND: Ketoacidosis is a severe metabolic complication mainly reported in diabetic patients. Therapeutic fasting is a millennial worldwide practice, believed to improve a large panel of health conditions, but its efficiency and safety profile have not yet been established. We report here a case of euglycemic ketoacidosis in a non-diabetic woman. CASE DESCRIPTION: A 51-year-old woman without a history of excessive alcohol use or medical history, except for a depressive disorder, was admitted in the emergency room for altered general status, deep asthenia, muscular weakness, articular pain, nausea, vomiting, and consciousness disorders. She was practicing during the previous 48 h a therapeutic fasting following a progressive restrictive diet for 4 d. She was diagnosed with ketoacidosis and hospitalized in the intensive care unit. Her laboratory test results indicated pH 7.28, bicarbonate 7 mmol/L, significant ketone bodies, glycemia 8.9 mmol/L without glycosuria, and negative blood alcohol assessment. Glycated hemoglobin was 5.5%, and blood glucose never went above 9 mmol/L. Serum concentrations of free fatty acids were high at 1.13 mmol/L (normal range: 0.13-0.45). Plasma insulin and peptide C were in the normal ranges. Comprehensive plasma and urinary biochemistry panels, including energetic substrates, and chromatography of amino acids and organic acids did not indicate any energetic or metabolic deficiency. The ketoacidosis regressed, and the overall outcome was favorable after intravenous glucose infusion for 48 h, without insulin requirement. CONCLUSIONS: This report is the first case, to our knowledge, of euglycemic ketoacidosis thought to be induced by therapeutic fasting in a non-diabetic patient. Practitioners should be aware of this complication of fasting.

Skin Autofluorescence of Pregnant Women With Diabetes Predicts the Macrosomia of Their Children.

Advanced glycation end products (AGEs) accumulated during long-term hyperglycemia are involved in diabetes complications and can be estimated by skin autofluorescence (sAF). During pregnancy, hyperglycemia exposes women to the risk of having a macrosomic newborn. The aim of this study was to determine whether sAF of women with diabetes during a singleton pregnancy could predict macrosomia in their newborns. Using an AGE Reader, we measured the sAF at the first visit of 343 women who were referred to our diabetology department during years 2011-2015. Thirty-nine women had pregestational diabetes, 95 early gestational diabetes mellitus (GDM), and 209 late GDM. Macrosomia was defined as birth weight ≥4,000 g and/or large for gestational age ≥90th percentile. Forty-six newborns were macrosomic. Their mothers had 11% higher sAF compared with other mothers: 2.03 ± 0.30 arbitrary units (AUs) vs. 1.80 ± 0.34 (P < 0.0001). Using multivariate logistic regression, the relation between sAF and macrosomia was significant (odds ratio 4.13 for 1-AU increase of sAF [95% CI 1.46-11.71]) after adjusting for several potential confounders. This relation remained significant after further adjustment for HbA1c (among 263 women with available HbA1c) and for women with GDM only. sAF of pregnant women with diabetes, a marker of long-term hyperglycemic exposure, predicts macrosomia in their newborns.