basal bolus
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2022 ◽  
Vol 22 (1) ◽  
Author(s):  
Franzisca Merkofer ◽  
Tristan Struja ◽  
Neele Delfs ◽  
Carlos C. Spagnuolo ◽  
Jason F. Hafner ◽  
...  

Abstract Background Glucocorticoid (GC)-induced hyperglycemia is a frequent adverse effect in hospitalized patients. Guidelines recommend insulin treatment to a target range of 6–10 mmol/L (108–180 mg/dl), but efficacies of particular regimes have not been well-studied. Methods In this retrospective cohort study, hospitalized patients receiving GCs at the medical ward were analyzed by treatment (basal-bolus vs. bolus-only vs. pre-mixed insulin) and compared to a non-insulin-therapy reference group. Coefficients of glucose variation (CV), percentage of glucose readings in range (4–10 mmol/L (72–180 mg/dl)) and hypoglycemia (< 4 mmol/L (< 72 mg/dl)) were evaluated. Results Of 2424 hospitalized patients receiving systemic GCs, 875 (36%) developed GC-induced hyperglycemia. 427 patients (17%) had a previous diagnosis of diabetes. Adjusted relative risk ratios (RRR) for the top tertile of CV (> 29%) were 1.47 (95% Cl 1.01–2.15) for bolus-only insulin, 4.77 (95% CI 2.67–8.51) for basal-bolus insulin, and 4.98 (95% CI 2.02–12.31) for premixed insulin, respectively. Adjusted RRR for percentages of glucose readings in range were 0.98 (95% Cl 0.97–0.99) for basal-bolus insulin, 0.99 (95% Cl 0.98–1.00) for premixed insulin, and 1.01 (95% Cl 1.00–1.01) for bolus-only insulin, respectively. Adjusted RRR for hypoglycemia was 13.17 (95% Cl 4.35–39.90) for basal-bolus insulin, 8.92 (95% Cl 2.60–30.63) for premixed insulin, and 2.99 (95% Cl 1.01–8.87) for bolus-only insulin, respectively. Conclusions Current guidelines recommend a basal-bolus regimen for treatment of GC-induced hyperglycemia, but we found similar outcomes with pre-mixed and bolus-only insulin regimens. As GC-induced hyperglycemia is a frequent issue in hospitalized patients, it might be reasonable to prospectively study the ideal regimen.


2021 ◽  
pp. 193229682110621
Author(s):  
Catherine Price ◽  
Gillian Ditton ◽  
Gregory B. Russell ◽  
Joseph Aloi

Background: Optimal inpatient glycemic management targets a blood glucose (BG) of 140-180 mg/dL and is an important safety measure for hospitalized patients with hyperglycemia. Traditional barriers to appropriate insulin administration include incorrect timing of prandial insulin administration, failure to administer basal insulin to persons with insulin deficiency/type 1 diabetes mellitus (DM), and inaccurate insulin dosing or timing resulting in hypoglycemia. Given the ongoing rapid assimilation of technology to manage our patients with DM, we investigated the use of continuous glucose monitoring (CGM) in the inpatient setting as a potential solution to traditional barriers to optimal hyperglycemia management for inpatient care. In this study, we evaluated the efficacy of use of inpatient CGM for insulin dosing in comparison with current standard of care and whether CGM could aid in minimizing hypoglycemic events. Methods: This study evaluated the use of Abbott professional (blinded) Freestyle Libre CGMs in participants treated with basal bolus insulin administered with subcutaneous insulin (basal bolus therapy [BBT]: n = 20) or on intravenous insulin (IVI) infusions (n =16) compared with standard point of care (POC) BG measurements. All participants on IVI were admitted with a diagnosis of diabetic ketoacidosis (DKA). The CGM data was not available in real time. Sensors were removed at the time of discharge and data uploaded to Libre View. Continuous BG data were aggregated for each subject and matched to POC BG or lab chemistry values within five minutes. The POC BG results were assessed for comparability (CGM vs standard BG testing). Data were further analyzed for clinical decision-making for correction insulin. Results: The overall mean absolute relative difference including both IVI and BBT groups was 22.3% (SD, 9.0), with a median of 20.0%. By group, the IVI arm mean was 19.6% (SD, 9.4), with a median of 16.0%; for BBT, the arm mean was 24.6% (SD, 8.1), with a median 23.4%. Using the Wilcoxon two-sample test, the means were not different ( P = .10), whereas the medians were ( P = .015). The CGM consistently reported lower glucose values than POC BG in the majority of paired values (BBT arm mean difference = 44.8 mg/dL, IVI mean difference = 19.7 mg/dL). Glucose results were in agreement for the group 83% of the time with Bland-Altman Plot of Difference versus the mean of all glucometric data. Analysis of correction dose insulin using either CGM or POC BG values resulted in a negligible difference in calculated insulin dose recommended in those receiving subcutaneous insulin. Corrective doses were based on weight and insulin sensitivity (type 1 vs type 2 DM). Participants initially on IVI were included in a data set of BBT once IVI therapy ceased and basal bolus insulin regimen was started. The data of all basal bolus therapy participants with 1142 paired values of CGM versus POC glucose were used. The dosing difference was less for CGM than POC BG in the majority of paired values, and there was an absolute difference in dose of insulin of only 1.34 units. In the IVI group with 300 paired values of CGM versus POC glucose, there was an absolute difference in dose of insulin of only 0.74 units. About a third of the patients studied in the BBT arm experienced a hypoglycemic event with POC BG <70 mg/dL. If used in real time, CGM would have identified a hypoglycemic event for our patients on average 3 hours and 34 minutes before it was detected by standard POC BG. Two participants incurred severe nocturnal hypoglycemia during the study with POC BG <54 mg/dL with hypoglycemia detected on CGM up to 3 hours and 42 minutes before POC testing. Conclusions: These results suggest that the use of inpatient CGM arrives at similar correction insulin dosing. The routine use of CGM for inpatients would consistently underestimate the BG compared with POC BG and could aid in minimizing and predicting hypoglycemia in the hospital setting. Our data support that the model of adoption of real-time inpatient CGM technology is anticipated to have significant impact in the clinical setting in efforts to maintain adequate glycemic control targeting BG 140-180 mg/dL while minimizing the frequency of hypoglycemic events.


2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Lucia Brodosi ◽  
Bianca Baracco ◽  
Vilma Mantovani ◽  
Loris Pironi

Abstract Background Maturity Onset Diabetes of the Young (MODY) is a monogenic, autosomal, dominant disease that results in beta-cells dysfunction with consequent hyperglycaemia. It represents a rare form of diabetes (1–2% of all the cases). Sulphonylureas (SUs) represent the first-line treatment for this form of diabetes mellitus. NEUROD1 is expressed by the nervous and the pancreatic tissues, and it is necessary for the proper development of beta cells. A neurogenic differentiation factor 1 (NEUROD1) gene mutation causes beta-cells dysfunction, inadequate insulin secretion, and hyperglycaemia (MODY 6). Case presentation We have documented a new missense mutation (p.Met114Leu c.340A > C) of the NEUROD1 gene, pathogenetic for diabetes mellitus, in a 48 years-old man affected by diabetes since the age of 25 and treated with insulin basal-bolus therapy. Unfortunately, an attempt to replace rapid insulin with dapagliflozin has failed. However, after the genetic diagnosis of MODY6 and treatment with SUs, he was otherwise able to suspend rapid insulin and close glucose monitoring. Interestingly, our patient had an early onset dilated cardiomyopathy, though no data about cardiac diseases in patients with MODY 6 are available. Conclusions Diagnostic criteria for MODY can overlap with other kinds of diabetes and most cases of genetic diabetes are still misdiagnosed as diabetes type 1 or 2. We encourage to suspect this disease in patients with a strong family history of diabetes, normal BMI, early-onset, and no autoimmunity. The appropriate therapy simplifies disease management and improves the quality of the patient’s life.


Author(s):  
Rujuta Patil

A clinical decision report using: Fulcher G, Roberts A, Sinha A, Proietto J. What happens when patients require intensification from basal insulin? A retrospective audit of clinical practice for the treatment of type 2 diabetes from four Australian centres. Diabetes Research and Clinical Practice, 2015;108(3):405–413. https://doi.org/10.1016/j.diabres.2015.03.004 for a patient with uncontrolled type 2 diabetes.


2021 ◽  
Vol 24 (3) ◽  
pp. 196
Author(s):  
Irace, C.

The basal-bolus insulin regimen in the management of diabetes is essential to achieve the recommended glycosylated hemoglobin (HbA1c) to reduce the incidence or the progression of chronic complications. HbA1c is influenced by either fasting plasma glucose and post-prandial hyperglycemia. Faster Aspart is an insulin Aspart with two additional excipients, L-arginine and niacinamide, which provide a faster subcutaneous absorption, the earlier onset of appearance, and consequently the optimization of post-prandial glucose control. Faster Aspart has been widely investigated in the ‘‘onset’’ clinical trials, which show better post-prandial glycemic excursions and noninferiority compared to insulin Aspart with HbA1c reduction. Clinical evidence demonstrates that faster Aspart is a therapeutic option able to provide clinical benefits over the current rapid-acting insulin analogs in terms of improved meal-related glycaemic control in subjects with diabetes. KEY WORDS post-prandial hyperglycemia; cardiovascular disease; insulin treatment; faster-acting insulin; faster aspart.


Author(s):  
Koushik Handattu ◽  
Lokesh Sharma ◽  
Kalasekhar Vijayasekharan ◽  
Vasudeva K ◽  
Shrikiran Aroor ◽  
...  

Corticosteroids and L-asparaginase used in the treatment of pediatric acute lymphoblastic leukemia (ALL) results in Drug induced Diabetes Mellitus (DIDM). Literature on the management of DIDM among children with ALL is sparse and the diagnostic criteria for pediatric diabetes should be carefully applied considering the acute and transient nature of DIDM during ALL therapy. Insulin remains the standard of care for DIDM management and the choice of Insulin regimen (standalone Neutral Protamine Hagedorn (NPH) or basal bolus) should be based on the type and dose of steroids used for ALL and the pattern of hyperglycemia. A modest glycemic control (140-180 mg/dl) to achieve euglycemia and prevent hypoglycemia would be the general approach. This review is intended to suggest a evidence based practical guidance in the diagnosis and management of DIDM during pediatric ALL therapy.


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