Steroids are drugs that have been used extensively in a variety of conditions. Although widely prescribed for their anti-inflammatory and immunosuppressive properties, glucocorticoids have several side effects, being hyperglycemia one of the most common and representative. In the present review, we discuss the main epidemiologic characteristics associated with steroid use, with emphasis on the identification of high risk populations. Additionally we present the pathophysiology of corticosteroid induced hyperglycemia as well as the pharmacokinetics and pharmacodynamics associated with steroid use. We propose a treatment strategy based on previous reports and the understanding of the mechanism of action of both, the different types of glucocorticoids and the treatment options, in both the ambulatory and the hospital setting. Finally, we present some of the recent scientific advances as well as some options for future use of glucocorticoids.

BackgroundGlucocorticoids commonly cause drug-induced diabetes. This association is well recognized but available evidence does not answer clinically relevant issues in subjects without diabetes.MethodsThirty-five individuals without diabetes with a recent diagnosis of acute lymphoblastic leukemia or non-Hodgkin’s lymphoma on high-dose glucocorticoid therapy were studied. Close systematic monitoring of fasting and postprandial glycemia and fasting insulin determinations, HOMA-insulin resistance and HOMA β-cell function were performed. The primary objective was to define the incidence of secondary diabetes in patients treated with high-dose glucocorticoids. Secondary objectives were to specify the intensity, the moment it appears and the evolution of hyperglycemia, in addition to the risk factors, mechanisms and impact of continuous and cyclical glucocorticoids on the development of hyperglycemia.ResultsMean age of patients was 38.4 ± 18.7 years. The incidence of diabetes was 40.6% and was found after the first week; half the time it occurred between the second and fourth. Two-thirds spontaneously normalized by eight weeks. Continuous glucocorticoid administration had a higher incidence of fasting hyperglycemia (P = 0.003). Mean peak insulin levels were significantly higher in cases of diabetes.ConclusionsHigh-dose prednisone for 2 to 3 months produced an elevated incidence of diabetes, usually with mild hyperglycemia occurring between the second and fourth week, normalizing spontaneously in all cases. Hyperglycemia was more frequent with continuous doses and occurred in cases with increased insulin resistance. The clinical and therapeutic characteristics of our participants, who were otherwise healthy, could represent the clinical setting of many patients with illness from other medical areas that might require high doses of GC for six to twelve weeks.

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Acute pancreatitis and diabetic ketoacidosis are unusual adverse events following chemotherapy based on L-asparaginase and prednisone as support treatment for acute lymphoblastic leukemia. We present the case of a 16-year-old Hispanic male patient, in remission induction therapy for acute lymphoblastic leukemia on treatment with mitoxantrone, vincristine, prednisone, and L-asparaginase. He was hospitalized complaining of abdominal pain, nausea, and vomiting. Hyperglycemia, acidosis, ketonuria, low bicarbonate levels, hyperamylasemia, and hyperlipasemia were documented, and the diagnosis of diabetic ketoacidosis was made. Because of uncertainty of the additional diagnosis of acute pancreatitis as the cause of abdominal pain, a contrast-enhanced computed tomography was performed resulting in a Balthazar C pancreatitis classification.

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BackgroundType 2 diabetes mellitus (T2DM) is a progressive chronic disease associated with severe microvascular and macrovascular complications.Our aim is to assess the real world effectiveness of SGT" inhibitors in achieving metabolic therapeutic goals.MethodsA retrospective, observational study. Inclusion criteria for patients were a previous diagnosis of type 2 diabetes mellitus, age > 18 years, patients receiving either dapagliflozin 10 mg and/or canagliflozin 300 mg. We excluded pregnant patients, patients with type 1 diabetes mellitus and acute metabolic complications of diabetes. Patients included in the analysis were enrolled in a health plan at least 6 months prior to the index date (baseline period) and in the 6 months following the index date (follow-up period). Achievement of glycated hemoglobin goals were established as <7%.ResultsWe screened 2870 Mexican patients; 288 (10.03% received SGLT2 inhibitors). Mean age for both groups of patients was 57.68 ± 11.06 years. The dapagliflozin control rate was 19.56% and the canagliflozin control rate 18.96%. Monotherapy with SGLT2 inhibitors was used in 21 patients (6.25%). Overall HbA1c goals were met in 56 patients (19.44%) with similar results with dapagliflozin or canagliflozin. The combination of SGLT2 inhibitors and sulfonylureas had the highest control rate (30.30%) compared to other regimens. Monotherapy was present in 6.25%. Insulin requirement was associated with poor control (2.8% vs. 18.05%, P < 0.05, 95% CI [0.07, 0.84]). Combination therapy with DPP4 inhibitors was associated with better control (P < 0.05, 95% CI, [1.10, 3.92]).ConclusionNo difference between the drugs was observed. Real-world effectiveness data of SGLT2 inhibitors show that the percentage of patients reaching metabolic goals is low. SLGT2 inhibitors were used more frequently as combined therapy.

Continuous monitoring systems are as useful as capillary monitoring for achieving normoglycemia.