Glucocorticoid-induced Hyperglycemia Research Articles

Analysis of Glucocorticoid-Related Genes Reveal CCHCR1 as a New Candidate Gene for Type 2 Diabetes.

Glucocorticoids have multiple therapeutic benefits and are used both for immunosuppression and treatment purposes. Notwithstanding their benefits, glucocorticoid use often leads to hyperglycemia. Owing to the pathophysiologic overlap in glucocorticoid-induced hyperglycemia (GIH) and type 2 diabetes (T2D), we hypothesized that genetic variation in glucocorticoid pathways contributes to T2D risk. To determine the genetic contribution of glucocorticoid action on T2D risk, we conducted multiple genetic studies. First, we performed gene-set enrichment analyses on 3 collated glucocorticoid-related gene sets using publicly available genome-wide association and whole-exome data and demonstrated that genetic variants in glucocorticoid-related genes are associated with T2D and related glycemic traits. To identify which genes are driving this association, we performed gene burden tests using whole-exome sequence data. We identified 20 genes within the glucocorticoid-related gene sets that are nominally enriched for T2D-associated protein-coding variants. The most significant association was found in coding variants in coiled-coil α-helical rod protein 1 (CCHCR1) in the HLA region (P = .001). Further analyses revealed that noncoding variants near CCHCR1 are also associated with T2D at genome-wide significance (P = 7.70 × 10–14), independent of type 1 diabetes HLA risk. Finally, gene expression and colocalization analyses demonstrate that variants associated with increased T2D risk are also associated with decreased expression of CCHCR1 in multiple tissues, implicating this gene as a potential effector transcript at this locus. Our discovery of a genetic link between glucocorticoids and T2D findings support the hypothesis that T2D and GIH may have shared underlying mechanisms.

Study rationale and design of the EANITIATE study (EmpAgliflozin compared to NPH Insulin for sTeroId diAbeTEs) - a randomized, controlled, multicenter trial of safety and efficacy of treatment with empagliflozin compared with NPH-insulin in patients with newly onset diabetes following initiation of glucocorticoid treatment

BackgroundA well-known metabolic side effect from treatment with glucocorticoids is glucocorticoid-induced diabetes mellitus (GIDM). Guidelines on the management of GIDM in hospitalized patients (in the non-critical care setting), recommend initiation of insulin therapy. The scientific basis and evidence for superiority of insulin therapy over other glucose lowering therapies is however poor and associated with episodes of both hypo- and hyperglycaemia. There is an unmet need for an easier, safe and convenient therapy for glucocorticoid-induced diabetes.MethodsEANITIATE is a Danish, open, prospective, multicenter, randomized (1:1), parallel group study in patients with new-onset diabetes following treatment with glucocorticoids (> 20 mg equivalent prednisolone dose/day) with blinded endpoint evaluation (PROBE design). Included patients are randomized to either a Sodium-Glucose-Cotransporter 2 (SGLT2) inhibitor or neutral protamin Hagedorn (NPH) insulin and followed for 30 days. Blinded continuous glucose monitoring (CGM) will provide data for the primary endpoint (mean daily blood glucose) and on glucose fluctuations in the two treatment arms. Secondary endpoints are patient related outcomes, hypoglycaemia, means and measures of variation for all values and for time specific glucose values. This is a non-inferiority study with the intent to demonstrate that treatment with empagliflozin is not inferior to treatment with NPH insulin when it comes to glycemic control and side effects.DiscussionThis novel approach to management of glucocorticoid-induced hyperglycemia has not been tested before and if SGLT2 inhibition with empaglifozin compared to NPH-insulin is a safe, effective and resource sparing treatment for GIDM, it has the potential to improve the situation for affected patients and have health economic benefits.Trial registrationwww.clinicaltrialsregister.eu no.: 2018–002640-82. Prospectively registered November 20th. 2018.Date of first patient enrolled: June 4th. 2019.This protocol article is based on the EANITATE protocol version 1.3, dated 29. January 2018.

SAT-640 Glycemic Profile of Intravenous Glucocorticoid Induced Hyperglycemia Using Continuous Glucose Monitoring

Background: Intravenous (IV) steroids are widely used in critically ill patients and with chemotherapy. It is well known that glucocorticoid-induced hyperglycemia (GCIH) occurs within 3 hours following oral administration of steroids with typical postprandial glycemic excursions lasting 24-36 hours. The recent increased availability of Continuous Glucose Monitoring (CGM) has allowed a detailed description of glycemic fluctuations in patients receiving steroids in different settings, however there is no reported observation of CGM findings following a single dose of IV Dexamethasone in a patient with diabetes. We present a case of glycemic pattern documented on CGM of a patient with type 2 diabetes, who had received 11 cycles of a single dose Dexamethasone-containing chemotherapy. Clinical Case: The patent is 70 years old female with history of type 2 DM of 19 years duration and metastatic pancreatic adenocarcinoma, diagnosed in November 2018, and treated with Fluorouracil and Dexamethasone 6mg IV on every other Wednesday since December 2018. Her diabetes was fairly controlled on Metformin, Repaglinide, Pioglitazone and Detemir insulin. Premeal Lispro was added while Metformin and Repaglinide were discontinued with the beginning of chemotherapy. She started using Freestyle Libre CGM in January 2019. During her visit in March 2019, the patient was taking Detemir Insulin 50 units in AM and 30 units at night, and Lispro 15 units before meals, in addition to correction insulin based on an Insulin Sensitivity Factor (ISF) of 1:25 for Blood Glucose (BG) above 200mg/dl. Unlike the reported postprandial hyperglycemic excursions associated with oral steroids, the patient’s CGM data showed a reproducible triphasic glycemic pattern following IV Dexamethasone, consisting of a steady state of hyperglycemia reached within 3 hours and lasting around 18-30 hours, followed by a transient BG improvement for 18-20 hours, and ending with another hyperglycemic plateau of 10-16 hours on day 3 post chemotherapy, with no association to meal intake. Given this recurrent pattern, the patient was advised to increase her bedtime Detemir insulin from 30 to 45 units and her correction ISF from 1:25 to 1:18 on days 1 and 2 after chemotherapy, with subsequent attenuation and shortening of GCIH. Conclusion: Our case report is the first one to describe CGM documented glycemic profile following a single dose of IV Dexamethasone in a patient with type 2 diabetes treated with insulin. The CGM data reveals a consistent steady GCIH, lasting around 48 hours, and reflecting the prolonged action of Dexamethasone. The transient BG improvement seen on day 2 is likely due to the Detemir dose self-increase and the carbohydrates intake decrease in response to day 1 hyperglycemia. A 48 hours modified insulin regimen based on higher dose of long acting and correction insulin improved Dexamethasone induced hyperglycemia.

Dulaglutide improves glucocorticoid-induced hyperglycemia in inpatient care and reduces dose and injection frequency of insulin

BackgroundGlucocorticoid (GC)-induced hyperglycemia is characterized by elevated postprandial blood glucose, which commonly requires multiple insulin injections. We investigated whether a long-acting glucagon-like peptide-1 receptor agonist, dulaglutide (Dula), safely improved GC-induced hyperglycemia in inpatients, to reduce insulin injection frequency.MethodsThe data of hospitalized patients with GC-induced hyperglycemia treated with Dula (Dula group, n = 38) or without (non-Dula group, n = 38) were retrospectively evaluated. Baseline data were collected at the beginning of GC treatment. The primary outcome in this study was glycemic control, which was compared between the groups using the six-point blood glucose (before and 2 h after each meal) profiles at discharge. The daily injection frequency of injectable drugs at discharge were also compared between groups.ResultsNo specific trend of underlying diseases was observed between the non-Dula and Dula groups. The proportion of patients previously administered with GC pulse therapy was comparable between the two groups. No significant differences were observed between groups, in the starting maintenance GC dose, GC dose at pretreatment of Dula and discharge, and cumulative GC dose during the observation. Six-point blood glucose levels at pretreatment and discharge were comparable between the two groups. However, daily injection frequency of injectable drugs and insulin dose were significantly lower in the Dula group than that in the non-Dula group. No differences were observed in the number of hypoglycemic events, the elevation of serum pancreatic enzyme levels, or gastrointestinal adverse events.ConclusionThese findings suggest that Dula could provide glycemic control while reducing the insulin dose and injection frequency in inpatients with GC-induced hyperglycemia. The occurrence of adverse events such as gastrointestinal symptoms and hypoglycemia did not increase in the Dula-treated patients compared to those not treated, suggesting its safety.

Efficacy and safety of alogliptin for glucocorticoid-induced hyperglycemia in patients with autoimmune-diseases: A retrospective analysis

Efficacy and safety of alogliptin for glucocorticoid-induced hyperglycemia in patients with autoimmune-diseases: A retrospective analysis

Glucocorticoid-induced hyperglycemia in oncohematological patients

Background Glucocorticoids are a common component of systemic chemotherapy regimens for hematological malignancy. Steroid-induced hyperglycemia remains a common potentially harmful problem that must be considered when using any type of glucocorticoids. Little is known about the impact of hyperglycemia associated with steroid use on treatment morbidity, infectious complications, as well as disease remission and mortality. Objective The aim of the current work is to study glucocorticoid-induced hyperglycemia in patients with hematologic malignancies receiving repeated short-term pulse cycles of glucocorticoids (5–7 days), to estimate its prevalence, to define the risk factors, and to assess treatment response. Patients and methods The prospective study included 30 adult patients with acute lymphoblastic leukemia, non-Hodgkin’s lymphoma, and chronic lymphocytic leukemia attending the outpatient clinic of Al Hussein Hospital, Al Azhar University during the period between November 2015 and April 2016. During the period of the study, 30 patients received a total of 60 cycles of chemotherapy including corticosteroid. Results Out of the 30 study patients, 15 (50%) were men and 15 (50%) were women with a mean age of 44.17. Corticosteroid-induced hyperglycemia was documented in 12 patients after one or more than one cycle (12/30–40%). Among the 60 cycles, corticosteroid-induced hyperglycemia was documented after 19 cycles (19/60–31%). The age of the patient was found to be the most important factor that affected the occurrence of hyperglycemia after corticosteroid where younger patients were less likely to develop hyperglycemia (P=0.013). Patients with BMI less than or equal to 25 had the lowest chance to develop hyperglycemia after corticosteroid. However, this difference was not statistically significant. The three patients who developed persistent hyperglycemia received hypoglycemic medications. Conclusion About one-third of patients with hematological malignancies receiving glucocorticoids may develop hyperglycemia. To allow for early detection and effective treatment, these patients should be screened for hyperglycemia at least before each cycle and 4–6 h after glucocorticoids intake, especially old obese patients Appropriate guidelines for the diagnosis and treatment of steroid-induced diabetes are needed in order to prevent complications associated with the hyperglycemic state

Diabetes mellitus and hyperglycemic complications in bullous pemphigoid

Diabetes mellitus and hyperglycemic complications in bullous pemphigoid

1028-P: Is Once-Weekly GLP-1 Receptor Agonist a Reasonable Option for Glucocorticoid-Induced Hyperglycemia? Twelve-Week Efficacy and Safety of Dulaglutide vs. Sitagliptin in Patients with Diabetes on Routine Glucocorticoid Treatment

Background: The efficacy and safety of incretin-based therapies for glucocorticoid-induced hyperglycemia, for which insulin is often used, remain to be established in real-world clinical settings. We aimed to study whether a once-weekly GLP-1 receptor agonist improves glycemic control in patients on glucocorticoid therapy compared with a DPP-4 inhibitor. Methods: We retrospectively compared the 12-week efficacy and safety of dulaglutide versus sitagliptin in patients with diabetes on prednisolone treatment (4-40 mg/day) who visited our hospital from 2015 to 2018. Results: Among 73 patients who started dulaglutide or sitagliptin for glucocorticoid-induced hyperglycemia while on prednisolone treatment (4-40 mg/day), 40 patients continued dulaglutide or sitagliptin along with prednisolone (4-40 mg/day) for the entire treatment period of 12 weeks (n =16, 24, respectively). The baseline characteristics and change in prednisolone doses from baseline to 1-12 weeks were comparable between the two groups. Dulaglutide significantly reduced the HbA1c and total daily insulin doses per bodyweight from baseline to 12 weeks (-0.78, p = 0.034; -0.29, p = 0.001, respectively), whereas neither was achieved by sitagliptin (-0.26, p = 0.088; -0.12, p = 0.105). A significantly higher proportion of patients were insulin-free at 12 weeks in the dulaglutide group than in the sitagliptin group (61.5% vs. 20.0%, p = 0.046). As for adverse events, nausea and vomiting were observed in 11.1% of the dulaglutide group. Hypoglycemia was not observed in either group. Conclusions: Compared with sitagliptin, dulaglutide can be an effective option for glucocorticoid-induced hyperglycemia with acceptable tolerability in real-world clinical settings. Disclosure S. Yoshiji: None. Y. Iwasaki: None. K. Iwasaki: None. M. Aizawa-Abe: None. S. Honjo: None. Y. Wada: None. J. Fujikawa: None. A. Hamasaki: None.

Assessment of the efficacy and safety of a protocol to manage glucocorticoid-induced hyperglycemia in diabetic patients during hospital stay

IntroductionThere are no agreed protocols on hospital management of hyperglycemic decompensation induced by pharmacological doses of glucocorticoids (GCs). The study objective was to assess the efficacy and safety of an insulin therapy protocol specific for patients treated with glucocorticoids (CP) as compared to a general protocol (GP) in diabetes decompensation secondary to glucocorticoids. Materials and methodsAn experimental study in patients with glucocorticoids-induced decompensated diabetes admitted to a respiratory ward including a non-randomized control group. Two protocols (CP and GP), both based on basal-bolo insulin regimens, but with different insulin doses and distribution, were compared.The difference in mean blood glucose (MBG) levels between both protocols was measured during hospital stay, as was the risk of having MBG levels>200mg/dL, adjusted for potential confounding factors (related to patients and to the glucocorticoid therapy used). ResultsA total of 131 patients were included, 60 assigned to the GP and 71 to the CP groups. Seventy-four percent of patients had been admitted due to COPD exacerbation. There was a significant difference in the total daily insulin dose used between the CP and GP groups (29.4 vs. 57.4 IU; p<0.0001).The adjusted difference in MBG levels (CP-GP) was −14.8 (95% CI, −26.2 to −3.3) mg/dL. Patients in the CP group had a lower adjusted risk of having MBG levels >200mg/dL during hospital admission (OR=0.31; 95% CI, 0.11–0.91; p=0.033). There were no differences in the risk of severe hypoglycemia between the CP and GP groups (0% vs. 1.4%; p=0.36). ConclusionsThe study protocol has been shown to decrease MBG levels in patients with glucocorticoids-induced decompensation of diabetes during hospital admission without compromising their safety.

Successful management of a glucocorticoid-induced hyperglycemia in hospitalized patient with use of novel protocol

Glucocorticoids can potentially cause hyperglycemia in otherwise normoglycemic individual or worsen the glycemic control in a patient having pre-existing diabetes mellitus. Management of glucocorticoid-induced hyperglycemia (GCIH) in hospitalized patients is a significant challenge. A recently published novel insulin protocol proposes the use of insulin neutral protamine Hagedorn (NPH) along with prednisolone to negate the hyperglycemic effect of prednisolone in a patient who develops GCIH. Here we report a case of an obese pre-diabetic female who developed GCIH following the use of prednisolone. The patient was initially managed with basal-bolus insulin protocol which leads to high glycemic variability. The use of single dose of insulin NPH along with the prednisolone as proposed by the novel protocol leads to excellent glycemic control while reducing glycemic variability. This case illustrates the use of the novel protocol in successful management.

Incidence of glucocorticoid-induced hyperglycemia among hospitalized nondiabetic patients

Searchable abstracts of presentations at key conferences in endocrinology ISSN 1470-3947 (print) | ISSN 1479-6848 (online)

Theophylline suppresses interleukin-6 expression by inhibiting glucocorticoid receptor signaling in pre-adipocytes

Adipose tissues in obese individuals are characterized by a state of chronic low-grade inflammation. Pre-adipocytes and adipocytes in this state secrete pro-inflammatory adipokines, such as interleukin 6 (IL-6), which induce insulin resistance and hyperglycemia. Theophylline (1,3-dimethylxanthine) exerts anti-inflammatory effects, but its effects on pro-inflammatory adipokine secretion by pre-adipocytes and adipocytes have not been examined. In this study, we found that theophylline decreased IL-6 secretion by 3T3-L1 pre-adipocytes and mouse-derived primary pre-adipocytes. The synthetic glucocorticoid dexamethasone (DEX) induced IL-6 expression in 3T3-L1 pre-adipocytes, and this effect was suppressed by theophylline at the mRNA level. Knockdown of CCAAT/enhancer binding protein (C/EBP) δ inhibited DEX-induced IL-6 expression, and theophylline suppressed C/EBPδ expression. Furthermore, theophylline suppressed transcriptional activity of the glucocorticoid receptor (GR) through suppression of nuclear localization of GR. In vivo, glucocorticoid corticosterone treatment (100 μg/mL) increased fasting blood glucose and plasma IL-6 levels in C57BL/6 N mice. Theophylline administration (0.1% diet) reduced corticosterone-increased fasting blood glucose, plasma IL-6 levels, and Il6 gene expression in adipose tissues. These results show that theophylline administration attenuated glucocorticoid-induced hyperglycemia and IL-6 production by inhibiting GR activity. The present findings indicate the potential of theophylline as a candidate therapeutic agent to treat insulin resistance and hyperglycemia.

Acute Hyperglycemia Associated with Anti-Cancer Medication.

Hyperglycemia during chemotherapy occurs in approximately 10% to 30% of patients. Glucocorticoids and L-asparaginase are well known to cause acute hyperglycemia during chemotherapy. Long-term hyperglycemia is also frequently observed, especially in patients with hematologic malignancies treated with L-asparaginase-based regimens and total body irradiation. Glucocorticoid-induced hyperglycemia often develops because of increased insulin resistance, diminished insulin secretion, and exaggerated hepatic glucose output. Screening strategies for this condition include random glucose testing, hemoglobin A1c testing, oral glucose loading, and fasting plasma glucose screens. The management of hyperglycemia starts with insulin or sulfonylurea, depending on the type, dose, and delivery of the glucocorticoid formulation. Mammalian target of rapamycin (mTOR) inhibitors are associated with a high incidence of hyperglycemia, ranging from 13% to 50%. Immunotherapy, such as anti-programmed death 1 (PD-1) antibody treatment, induces hyperglycemia with a prevalence of 0.1%. The proposed mechanism of immunotherapy-induced hyperglycemia is an autoimmune process (insulitis). Withdrawal of the PD-1 inhibitor is the primary treatment for severe hyperglycemia. The efficacy of glucocorticoid therapy is not fully established and the decision to resume PD-1 inhibitor therapy depends on the severity of the hyperglycemia. Diabetic patients should achieve optimized glycemic control before initiating treatment, and glucose levels should be monitored periodically in patients initiating mTOR inhibitor or PD-1 inhibitor therapy. With regard to hyperglycemia caused by anti-cancer therapy, frequent monitoring and proper management are important for promoting the efficacy of anti-cancer therapy and improving patients' quality of life.

Comparison of Two Protocols in the Management of Glucocorticoid-induced Hyperglycemia among Hospitalized Patients.

Context:There is limited literature focusing on the management of glucocorticoid-induced hyperglycemia (GCIH).Aims:The primary objective was to compare the mean blood glucose between the experimental group (new protocol) and the control group (standard protocol) in the management of GCIH. The secondary objective was to compare other parameters of glycemic efficacy, variability, and safety parameters.Methods:This was a randomized, open-labeled, parallel arm trial. Adult patients who were given glucocorticoid (minimum dose equivalent to prednisolone 10 mg) in the past 24 h and had 2 h postmeal plasma glucose ≥200 mg/dl were included in the study. Patients randomized to control group received standard basal-bolus insulin. In the experimental group, a “correctional insulin” matching the glycemic profile of the glucocorticoid administered was provided with or without “background” basal-bolus insulin. The parameters of glycemic efficacy, variability, and safety were compared. P < 0.05 was considered statistically significant.Results:Data of 67 patients included in the study were analyzed, of which 33 patients were in the experimental group and 34 patients in the control group. The mean blood glucose in the experimental and the control group was 170.32 ± 33.46 mg/dl and 221.05 ± 49.72, respectively (P = 0.0001). The parameters for glycemic variability were all significantly lower in patients in the experimental group. The hypoglycemia event rate was low in both the groups.Conclusion:When compared to the standard basal-bolus insulin protocol, the new protocol showed lower mean blood glucose and lower glycemic variability.

Abordagem e Tratamento da Hiperglicemia Induzida por Glicocorticóides

Glucocorticoids have been associated to several side effects, specially a diabetogenic action, the most common and representative effect. Glucocorticoid-induced hyperglycemia is a common medical condition, with general associated morbidity and mortality. It was performed a literature review about the management and treatment of glucocorticoid-induced hyperglycemia. Through numerous not quite fully understood mechanics, glucocorticoids promote hyperglycemia in non-diabetic patients and worsen diabetes control in diabetic individuals. Glucocorticoid-induced hyperglycemia presents key patterns, enhanced in the postprandial period and scheduled-dependent. Despite the existence of guidelines for hyperglycemia treatment in non-critic hospitalized and non-hospitalized patients, there are no guidelines respecting glucocorticoid-induced hyperglycemia. Nevertheless, it is known that glucocorticoid-induced hyperglycemia is complex and demanding, requiring a specific approach. Indeed, glucocorticoid-induced hyperglycemia treatment depends on the glucocorticoid used, its dose, frequency and schedule. Furthermore, the scheme of treatment previously used by diabetic individuals also influences the choice of the new scheme. The authors reviewed the glucocorticoid induced-hyperglycemia thematic and propose strategies to approach and treat glucocorticoid induced-hyperglycemia in diabetic and non-diabetic individuals. This review is expected to be useful in different settings and crosswise to all medical specialties.

Diabetology and oncology meet in a network model: union is strength.

Diabetes and cancer are increasingly common conditions, and the management of cancer patients with diabetes is often challenging. Diabetes in cancer patients poses several complex clinical issues, including which treatment is suitable to control hyperglycemia, how to better counteract glucocorticoid-induced hyperglycemia, and how to manage nutritional problems of cachectic patients and glucose variability linked to artificial nutrition. A key aspect to consider is the patients' position on the trajectory of the oncologic disease, both to establish which level of glycemic control should be pursued and to decide the most suitable antidiabetic treatment to recommend. Endocrinologists are rarely involved in the management of patients with advanced cancer. Furthermore, lack of guidelines results in a "trial-and-error" approach, often with suboptimal disease management. Lastly, cancer survivors represent a frequently underestimated category of patients at higher cardiometabolic risk. A practical solution for these challenges lies in the implementation of care networks based on a close partnership and ongoing communication between oncologists, endocrinologists, and nutritionists, placing the patient at the center of the care process. At the same time, universities and scientific societies should play a key role in promoting research into areas of intersection of oncology and endocrinology, in raising awareness of common possibilities of primary and secondary prevention of metabolic and oncologic diseases, as well as specific challenges of managing diabetes and cancer, and proper training of health workers, while also supporting the shared implementation of effective management strategies.

Hospital Insulin Protocol Aims For Glucose Control In Glucocorticoid-Induced Hyperglycemia

To compare the effectiveness of 2 insulin protocols to treat glucocorticoid-induced hyperglycemia in the nonintensive care hospital setting. A randomized, open-label, parallel-arm study was conducted comparing standard recommended care of complete insulin orders (CIO) (i.e., 3-part insulin regimen of long-acting basal [background], rapid-acting bolus [mealtime], and rapid-acting correction factor) to an experimental group following a regimen of Neutral Protamine Hagedorn (NPH) plus CIO (NPH-CIO). The primary outcome was mean blood glucose (BG), and the secondary outcome was percent of BG in target range of 70 to 180 mg/dL. Hypoglycemia was also evaluated. Sixty-one patients completed 2 to 5 consecutive inpatient days (31 CIO; 30 NPH-CIO). Baseline mean BG results were 237.2 ± 50.2 and 221.9 ± 35.8 mg/dL (P = .30) in the CIO and NPH-CIO groups, respectively. No significant difference in overall mean BG between the 2 groups was detected; however, a significant difference arose on day 3: mean BG 181.8 ± 32.6 mg/dL (CIO) versus 157.2 ± 6.1 mg/dL (NPH-CIO) (P = .03). Moreover, the total daily doses (TDDs) of insulin did not differ: 34.8 ± 43.0 units (CIO) versus 35.8 ± 25.0 units (NPH-CIO) (P = .13). Percent of BG in target was 54.6% (CIO) and 62% (NPH-CIO) (P = .24). Incidence of severe hypoglycemia (<50 mg/dL) was the same in both groups (0.1%). NPH added to 3-part insulin regimen (CIO) may be an effective way to a combat glucocorticoid-induced hyperglycemia, though further research is needed in a larger population.

Глюкокортикоид-индуцированные нарушения углеводного обмена: патогенез, диагностика. Есть ли повод волноваться, назначая пульс-терапию при эндокринной офтальмопатии?

Глюкокортикоид-индуцированные нарушения углеводного обмена: патогенез, диагностика. Есть ли повод волноваться, назначая пульс-терапию при эндокринной офтальмопатии?

Randomized clinical trial of the efficacy and safety of insulin glargine vs. NPH insulin as basal insulin for the treatment of glucocorticoid induced hyperglycemia using continuous glucose monitoring in hospitalized patients with type 2 diabetes and respiratory disease

AimsTo investigate the clinical efficacy and safety of insulin glargine compared with NPH insulin as basal insulin for the management of corticosteroid-induced hyperglycemia in hospitalized people with type 2 diabetes (T2DM) and respiratory disease. Materials and methodsRandomized, two-arm parallel group, clinical trial undertaken from February 2011 to November 2012 on the pneumology ward of the Hospital Regional Universitario de Málaga (Spain), involving 53 participants with T2DM treated with medium/high doses of intermediate-acting corticosteroids. Participants were randomly assigned to receive one single dose of insulin glargine or NPH insulin in three equally divided doses before each meal as basal insulin within a basal–bolus insulin protocol. The intervention lasted six days or until discharge if earlier. ResultsNo significant differences were seen between groups during the study in mean blood glucose (11.43±3.44mmol/l in glargine vs. 11.88±2.94mmol/l in NPH, p=0.624), and measures of glucose variability (standard deviation 3.27±1.16mmol/l vs. 3.61±0.99mmol/l, p=0.273; coefficient of variation 1.55±0.33mmol/l vs. 1.72±0.39mmol/l, p=0.200). Results from CGM were concordant with those obtained with capillary blood glucose reading. The length of hospital stay was also similar between groups (8.2±2.8 days vs. 9.8±3.4 days, p=0.166) There was a non significant trend for lower episodes of mild (4 vs. 8, p=0.351) and severe hypoglycemia (0 vs. 3, p=0.13) in the glargine group. ConclusionsThe results of this study showed that insulin glargine and NPH insulin are equally effective in a basal–bolus insulin protocol to treat glucocorticoid-induced hyperglycemia in people with T2DM on a pneumology ward.

Hyperglycemia in patients with hematologic malignancies.

Patients with hematologic malignancies are at high risk for hyperglycemia due to factors such as frequent exposure to glucocorticoids, immunosuppressants, total parenteral nutrition, and medical stress. Hyperglycemia in these patients has been associated with poor outcomes including increased risk of infection, organ dysfunction, durability of remission, graft-versus-host disease, and mortality. However, the appropriate glucose targets are not well established, and there are few prospective data assessing whether glucose control improves outcomes. HbA1c should be interpreted with caution in patients with hematologic malignancies, due to inaccuracies imposed by disordered hematopoiesis and frequent transfusions, and short-term perturbations imposed by acute illness or medications. Management of diabetes or glucocorticoid-induced hyperglycemia in the hospital generally requires insulin therapy, which is tailored based upon nutritional needs, baseline glucose control, and concomitant factors such as type and dose of glucocorticoid administration. Close follow-up and adjustment of therapy, ideally with the assistance of patient self-titration algorithms, is required after discharge. Patients are at increased long-term risk for developing diabetes and therefore should undergo regular screening.