Tuberculosis (TB) is a global health challenge with millions of
new cases and deaths annually world-wide. According to the
2020 WHO report, about 6 million new and relapsed cases
were diagnosed with about 160,000 cases laboratory-
confirmed cases with multidrug-resistant tuberculosis (MDR-
TB)/relapsing TB (/RR-TB).1 As for Egypt in 2020, about 7000
new and relapsed cases were diagnosed with 85% of the
bacteriologically confirmed new pulmonary TB cases tested
for rifampicin resistance were resistant.2
Rifampicin is an efficient drug for treatment of tuberculosis.
It has been prescribed as the first-line treatment in drug-
susceptible TB patients as well as in isoniazid resistant TB
patients. 3 It acts on the RNA polymerase and the rpoB gene is
the encoding gene.4 About 25 out of 34 mutations in that gene
have been found linked to the rifampicin resistan-
ce.5 Multidrug-resistant tuberculosis is defined as resistance to
rifampicin and isoniazid with many contributing reasons.

COVID-19 can be accompanied by acute neu-
rological complications of both central and peripheral ner-
vous systems (CNS and PNS). In this study, we estimate the
frequency of such complications among hospital inpatients
with COVID-19 in Assiut and Aswan university hospitals. Ma-
terials and Methods: We screened all patients with suspect-
ed COVID-19 admitted from 1 June to 10 August 2020 to the
university hospitals of Assiut and Aswan in Upper Egypt.
Clinical and laboratory tests, CT/MRI of the chest and brain,

Purpose The treatment landscape for chronic myeloid leukemia (CML) has been revolutionized by the introduction of imatinib, a tyrosine kinase inhibitor, which has transformed the disease from a fatal condition into a manageable chronic illness for a substantial number of patients. Despite this, some individuals do not respond adequately to the treatment, and others may experience disease progression even with continued therapy. This study examined how CYP2C8*3 (G416A; rs11572080) and ABCG2 C421A (rs2231142) single nucleotide polymorphisms (SNPs) affect the plasma trough concentration and therapeutic response of imatinib in Egyptian CML patients.
Methods The study included fifty patients with chronic-phase CML, who were categorized into two groups: responders (n = 26) and non-responders (n = 24), according to their BCR-ABL1 transcription levels after 12 months of imatinib treatment. Genotyping of the CYP2C8*3 and ABCG2 C421A polymorphisms was performed using polymerase chain reaction restriction fragment length polymorphism (PCR-RFLP), while plasma trough concentrations were determined through high performance liquid chromatography with ultraviolet-diode array detection (HPLC-UV/DAD).
Results Patients with the CA genotype of ABCG2 C421A showed significantly higher mean plasma trough concentrations of imatinib (CA: 1731 ± 424.7 ng/mL; CC: 1294 ± 381.3 ng/mL; p = 0.0132) and demonstrated a better molecular response compared to those with the CC genotype (p = 0.0395).
Conclusion The ABCG2 C421A polymorphism significantly influenced imatinib plasma trough concentrations and molecular responses in Egyptian chronic-phase CML patients. Genotyping of this polymorphism in these patients could assist in optimizing imatinib therapy, predicting more favorable treatment outcomes, and enabling the development of more personalized treatment plans.