scholarly journals Granulocyte-Colony Stimulating Factor (G-CSF) for stroke: an individual patient data meta-analysis

2016 ◽  
Vol 6 (1) ◽  
Author(s):  
Timothy J. England ◽  
Nikola Sprigg ◽  
Andrey M. Alasheev ◽  
Andrey A. Belkin ◽  
Amit Kumar ◽  
...  
Keyword(s):  
Individual Patient Data ◽  
Meta Analysis ◽  
Patient Data ◽  
Granulocyte Colony Stimulating Factor ◽  
Colony Stimulating Factor ◽  
Stimulating Factor ◽  
Factor G

scholarly journals SUN-424 Treatment of Antithyroid Drug-Induced Agranulocytosis with Granulocyte Colony-Stimulating Factor: A Meta-Analysis

2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Maria Regina C Santos ◽  
Christian Emmanuel T Lim ◽  
Ramon Jason M Javier ◽  
Alma R Calavera
Keyword(s):  
Primary Outcome ◽  
Meta Analysis ◽  
Antithyroid Drug ◽  
Mean Difference ◽  
Antithyroid Drugs ◽  
Granulocyte Colony Stimulating Factor ◽  
Colony Stimulating Factor ◽  
Drug Induced ◽  
Stimulating Factor ◽  
Factor G

Abstract BACKGROUND: Hyperthyroidism, a common condition seen by physicians, is predominantly treated with antithyroid drugs. Agranulocytosis, a potentially fatal complication, is their most serious side effect. Conflicting studies are present between the risks and benefits of the use of exogenous granulocyte colony-stimulating factor (G-CSF) in its treatment, since its pathogenesis has not been established. The objective of this study is to determine the benefit of G-CSF in antithyroid drug-induced (ATD) agranulocytosis, through a meta-analysis. Methods: Studies were included after extensive literature search in five electronic databases; all met the inclusion and exclusion criteria, and were critically appraised. The primary outcome was days to hematologic recovery, defined as neutrophilic rise to >0.5 x 109/L. Data were treated as continuous data, obtaining the standard mean difference through a Forrest Plot using the Review Manager 5.3 application. Results: Five of the studies were non-concurrent cohort, while one was a randomized clinical trial. The duration of the studies was from 1970s to 2014. Age range of the population was from 8 to 87 years old, with more females. G-CSF dose ranged from 75 to 300ug/day, injected subcutaneously or intramuscularly. Primary outcome measured common to all the studies included hematologic recovery. Five of the six studies showed shorter number of days to hematologic recovery for the treatment group compared to the control group (with a standardized mean difference of 1 day, confidence interval (CI) of 0.45 to 1.54). Conclusion: Exogenous G-CSF administration in ATD agranulocytosis contributed to faster hematologic recovery in terms of days, shortening recovery by a mean of 1 day. References: 1. Tamai, H., et al. Treatment of methimazole-induced agranulocytosis using recombinant human granulocyte colony-stimulating factor (rhG-CSF). J Clin Endocrinol Metab. 1993;77(5):1356-1360. 2. Andres, E., et al. Haematopoietic growth factor in antithyroid-drug-induced agranulocytosis. Q J Med. 2001;94:423-428. 3. Fukata, S., Kuma, K., Sugawara, M. Granulocyte colony-stimulating factor (G-CSF) does not improve recovery from antithyroid drug-induced agranulocytosis: a prospective study. Thyroid. 1999;9(1):29-31. 4. Tajiri, J., Noguchi, S. Antithyroid drug-induced agranulocytosis: how has granulocyte colony-stimulating factor changed therapy? Thyroid. 2005;15(3):292-297. 5. Watanabe, N., et al. Antithyroid drug-induced hematopoietic damage: a retrospective cohort study of agranulocytosis and pancytopenia involving 50,385 patients with Graves’ disease. J Clin Endocrinol Metab. 2012;97(1):E49-E53. 6. Clauna-Lumanta, M.M., Yao, C., Bolinao, J.F. The effects of GCSF on the recovery time and duration of hospitalization in patients with anti-thyroid drug-induced agranulocytosis in a tertiary hospital. JAFES. 2016;31(2):131-136.

scholarly journals Can granulocyte colony stimulating factor (G-CSF) ameliorate acetaminophen-induced hepatotoxicity?

2021 ◽  
pp. 096032712110085
Author(s):  
EA Ahmed ◽  
AM Abd-Eldayem ◽  
E Ahmed
Keyword(s):  
Liver Damage ◽  
Liver Toxicity ◽  
Serum Levels ◽  
Hepatic Tissue ◽  
Granulocyte Colony Stimulating Factor ◽  
Colony Stimulating Factor ◽  
Oxidative Markers ◽  
Stimulating Factor ◽  
New Strategies ◽  
Factor G

Acetaminophen (APAP) is often used as an antipyretic and analgesic agent. Overdose hepatotoxicity, which often results in liver cell failure and liver transplantation, is a severe complication of APAP usage. To save the liver and save lives from acute liver damage caused by APAP, the search for new strategies for liver defense is important. Wistar rats have been used for the induction of APAP hepatotoxicity. Elevated levels of serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP) and lactate dehydrogenase (LDH) were evaluated for liver toxicity. In addition, the levels of hepatic tissue oxidative markers such as malondialdehyde (MDA), nitric oxide (NO) increased while glutathione (GSH) was depleted and catalase (CAT) activity was curtailed. The biochemical findings were consistent with the changes in histology that suggested liver damage and inflammation. Treated rats with N-acetylcysteine (N-AC) and granulocyte colony stimulating factor (G-CSF) showed a decrease in serum levels of ALT, AST and LDH, while the level of ALP in the G-CSF group was still high. After administration of APAP, treatment with N-AC or G-CSF substantially reduced the level of MDA and NO while maintaining the GSH content and CAT activity. Treatment with N-AC and G-CSF after administration of APAP has also attenuated inflammation and hepatocytes necrosis. The results of this study showed that G-CSF could be viewed as an alternative hepatoprotective agent against APAP-induced acute liver injury compared to N-AC.

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