مقالات پذیرفته شده در نهمین کنگره بین المللی زیست پزشکی
A review of hemolytic anemia associated with glucose-6-phosphate dehydrogenase deficiency caused by the antibiotic
A review of hemolytic anemia associated with glucose-6-phosphate dehydrogenase deficiency caused by the antibiotic
Nastaran Bozorgi,1,*
1. Department of Biology, Faculty of Science, Shahid Chamran University of Ahvaz, Ahvaz, Iran
Introduction: Chloramphenicol and its derivatives (CAPs) are a class of bacteriostatic antibiotics that are effective against infections caused by a wide range of gram-negative (including Enterobacteriaceae) and gram-positive bacteria. This antibiotic was first isolated in Venezuela in 1947 from a microorganism known as Streptomyces venezuelae. Today, it is chemically synthesized and can be administered either by injection or orally. Chloramphenicol is critical in treating meningitis and is often used intramuscularly as a "last resort" when other antibiotics fail to effectively treat infections caused by multidrug-resistant (MDR) strains. The mechanism of action for chloramphenicol is selective, as it does not affect eukaryotic cells. It acts on the 50S subunit of the bacterial ribosome, preventing transpeptidation, which interrupts mRNA translation and protein synthesis, thus exerting its antibacterial effect. Research indicates that a deficiency in the enzyme glucose-6-phosphate dehydrogenase (G6PD) can lead to hemolytic anemia in individuals taking this medication. In hemolytic anemia, red blood cells deteriorate more quickly than the body can produce new ones, potentially resulting in serious complications such as heart arrhythmias, heart failure, and cardiomyopathy. As personalized medicine and precise therapeutic approaches at the molecular level become increasingly important, this study aims to investigate the deficiency in the G6PD enzyme and its role in the red blood cell breakdown of individuals taking chloramphenicol.
Methods: Keywords like Hemolytic anemia, glucose-6-phosphate dehydrogenase, and hloramphenicol. antibiotics were used to search scientific databases such as Google Scholar and PubMed. This led to the selection and review of relevant articles.
Results: Recent pharmacogenetic research has demonstrated that individuals with different genotypes can respond differently to the same medications. Pharmacogenetics is the study of how genetic variations affect people's reactions to drugs. Evidence shows that a deficiency in the G6PD enzyme is linked to the harmful effects of chloramphenicol antibiotics. This enzyme deficiency is the most common genetic abnormality, affecting more than 400 million people worldwide. The Gd gene, which is associated with the G6PD enzyme, is located on the long arm of the X chromosome. As a result of X-linked inheritance, men are more frequently affected by this condition than women. Deficiency of this enzyme is commonly found in tropical and subtropical regions. The mutation pattern associated with this enzyme involves point mutations at the nucleotide level, which do not fully inactivate the enzyme. The G6PD enzyme is present in all human cells and plays a crucial role in protecting cells from damage caused by reactive oxygen species. In cases of G6PD deficiency, the use of the antibiotic chloramphenicol can lead to the accumulation of oxidative substances within the cells. Given the critical role of red blood cells in oxygen transport, this accumulation can impair cellular respiration and protein production in the mitochondria, ultimately reducing overall energy levels in the cells. This process can lead to apoptosis, specifically in red blood cells.
Conclusion: To prevent negative reactions to antibiotics, doctors must prescribe appropriate medications and personalized treatment methods based on the patient’s condition, age, and genetic background. For infants with a family history of jaundice and adults showing symptoms such as an enlarged spleen, dark urine, and paleness, it is essential to conduct pharmacogenetic tests. By interpreting the results and applying tailored medical strategies, healthcare providers can initiate antibiotic treatment with the correct dosage. For patients with mild symptoms, discontinuing antibiotic use may be sufficient. However, in cases of more severe side effects, serious complications can be mitigated through blood transfusions or the administration of red blood cells.