Displaying all 4 publications

Abstract:
Sort:
  1. Hong JGS, Tan PC, Kamarudin M, Omar SZ
    BMC Pregnancy Childbirth, 2021 Feb 15;21(1):138.
    PMID: 33588801 DOI: 10.1186/s12884-021-03628-5
    BACKGROUND: Antenatal corticosteroids (ACS) are increasingly used to improve prematurity-related neonatal outcome. A recognized and common adverse effect from administration of antenatal corticosteroid is maternal hyperglycemia. Even normal pregnancy is characterized by relative insulin resistance and glucose intolerance. Treatment of maternal hyperglycemia after ACS might be indicated due to the higher risk of neonatal acidosis which may coincide with premature birth. Metformin is increasingly used to manage diabetes mellitus during pregnancy as it is effective and more patient friendly. There is no data on prophylactic metformin to maintain euglycemia following antenatal corticosteroids administration.

    METHODS: A double blind randomized trial. 103 women scheduled to receive two doses of 12-mg intramuscular dexamethasone 12-hour apart were separately randomized to take prophylactic metformin or placebo after stratification according to their gestational diabetes (GDM) status. First oral dose of allocated study drug was taken at enrolment and continued 500 mg twice daily for 72 hours if not delivered. Six-point blood sugar profiles were obtained each day (pre- and two-hour post breakfast, lunch and dinner) for up to three consecutive days. A hyperglycemic episode is defined as capillary glucose fasting/pre-meal ≥ 5.3 mmol/L or two-hour post prandial/meal ≥ 6.7 mmol/L. Primary outcome was hyperglycemic episodes on Day-1 (first six blood sugar profile points) following antenatal corticosteroids.

    RESULTS: Number of hyperglycemic episodes on the first day were not significantly different (mean ± standard deviation) 3.9 ± 1.4 (metformin) vs. 4.1 ± 1.6 (placebo) p = 0.64. Hyperglycemic episodes markedly reduced on second day in both arms to 0.9 ± 1.0 (metformin) vs. 1.2 ± 1.0 (placebo) p = 0.15 and further reduced to 0.6 ± 1.0 (metformin) vs. 0.7 ± 1.0 (placebo) p = 0.67 on third day. Hypoglycemic episodes during the 3-day study period were few and all other secondary outcomes were not significantly different.

    CONCLUSIONS: In euglycemic and diet controllable gestational diabetes mellitus women, antenatal corticosteroids cause sustained maternal hyperglycemia only on Day-1. The magnitude of Day-1 hyperglycemia is generally low. Prophylactic metformin does not reduce antenatal corticosteroids' hyperglycemic effect.

    TRIAL REGISTRATION: The trial is registered in the ISRCTN registry on May 4 2017 with trial identifier https://doi.org/10.1186/ISRCTN10156101 .

    Matched MeSH terms: Hyperglycemia/chemically induced
  2. Rama Chandran S, A Vigersky R, Thomas A, Lim LL, Ratnasingam J, Tan A, et al.
    Diabetes Technol Ther, 2020 02;22(2):103-111.
    PMID: 31502876 DOI: 10.1089/dia.2019.0277
    Background:
    Complex changes of glycemia that occur in diabetes are not fully captured by any single measure. The Comprehensive Glucose Pentagon (CGP) measures multiple aspects of glycemia to generate the prognostic glycemic risk (PGR), which constitutes the relative risk of hypoglycemia combined with long-term complications. We compare the components of CGP and PGR across type 1 and type 2 diabetes.
    Methods:
    Participants: n = 60 type 1 and n = 100 type 2 who underwent continuous glucose monitoring (CGM). Mean glucose, coefficient of variation (%CV), intensity of hypoglycemia (INThypo), intensity of hyperglycemia (INThyper), time out-of-range (TOR <3.9 and >10 mmol/L), and PGR were calculated. PGR (median, interquartile ranges [IQR]) for diabetes types, and HbA1c classes were compared.
    Results:
    While HbA1c was lower in type 1 (type 1 vs. type 2: 8.0 ± 1.6 vs. 8.6 ± 1.7, P = 0.02), CGM-derived mean glucoses were similar across both groups (P > 0.05). TOR, %CV, INThypo, and INThyper were all higher in type 1 [type 1 vs. type 2: 665 (500, 863) vs. 535 (284, 823) min/day; 39% (33, 46) vs. 29% (24, 34); 905 (205, 2951) vs. 18 (0, 349) mg/dL × min2; 42,906 (23,482, 82,120) vs. 30,166 (10,276, 57,183) mg/dL × min2, respectively, all P 
    Matched MeSH terms: Hyperglycemia/chemically induced
  3. Hasan SS, Kow CS, Bain A, Kavanagh S, Merchant HA, Hadi MA
    Expert Opin Pharmacother, 2021 Feb;22(2):229-240.
    PMID: 33054481 DOI: 10.1080/14656566.2020.1837114
    INTRODUCTION: Diabetes mellitus is one of the most prevalent comorbidities identified in patients with coronavirus disease 2019 (COVID-19). This article aims to discuss the pharmacotherapeutic considerations for the management of diabetes in hospitalized patients with COVID-19.

    AREAS COVERED: We discussed various aspects of pharmacotherapeutic management in hospitalized patients with COVID-19: (i) susceptibility and severity of COVID-19 among individuals with diabetes, (ii) glycemic goals for hospitalized patients with COVID-19 and concurrent diabetes, (iii) pharmacological treatment considerations for hospitalized patients with COVID-19 and concurrent diabetes.

    EXPERT OPINION: The glycemic goals in patients with COVID-19 and concurrent type 1 (T1DM) or type 2 diabetes (T2DM) are to avoid disruption of stable metabolic state, maintain optimal glycemic control, and prevent adverse glycemic events. Patients with T1DM require insulin therapy at all times to prevent ketosis. The management strategies for patients with T2DM include temporary discontinuation of certain oral antidiabetic agents and consideration for insulin therapy. Patients with T2DM who are relatively stable and able to eat regularly may continue with oral antidiabetic agents if glycemic control is satisfactory. Hyperglycemia may develop in patients with systemic corticosteroid treatment and should be managed upon accordingly.

    Matched MeSH terms: Hyperglycemia/chemically induced
  4. Nahar N, Mohamed S, Mustapha NM, Lau S, Ishak NIM, Umran NS
    Naunyn Schmiedebergs Arch Pharmacol, 2021 Mar;394(3):457-467.
    PMID: 33047165 DOI: 10.1007/s00210-020-01989-w
    Diabetes mellitus (DM) often causes ocular disorders leading to vision loss. Metformin is commonly prescribed for type 2 diabetes. This study assessed the effect of metformin on hyperglycemic histopathological eye abnormalities and some possible pathways involved. Male rats were divided into 3 groups (N = 6), namely, healthy control, hyperglycemic non-treated control, and hyperglycemic rats treated with 200 mg/kg metformin. Two weeks after diabetes induction by an intraperitoneal streptozotocin (60 mg streptozotocin (STZ)/kg) injection, the rats develop ocular abnormalities, and metformin (200 mg/kg) treatment was administered daily. Rats underwent dilated retinal digital ophthalmoscope examination and graded for diabetic retinopathy. Rats were sacrificed at 12 weeks, and the cornea, lens, sclera, ciliary body, iris, conjunctiva, retinal, and optic nerve were examined histologically. Rats' fasting blood glucose and body weight were monitored. Serum tumor necrosis factor-α (TNF-α), vascular endothelial growth factor (VEGF), claudin-1, and glutathione/malondialdehyde ratios were analyzed. Metformin significantly attenuated diabetes-related histopathological ocular deteriorations in the cornea, lens, sclera, ciliary body, iris, conjunctiva, retina, and optic nerve partly by restoring serum TNF-α, VEGF, claudin-1, and glutathione/malondialdehyde ratios without significantly affecting the fasting blood glucose levels or body weight in these hyperglycemic rats. Metformin attenuated hyperglycemia-associated histopathological eye deteriorations, possibly partly by ameliorating vascular leakage, oxidative stress, inflammation, and neovascularization, without affecting the fasting blood glucose levels or body weights in these STZ-induced diabetic rats.
    Matched MeSH terms: Hyperglycemia/chemically induced
Filters
Contact Us

Please provide feedback to Administrator (afdal@afpm.org.my)

External Links