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RISS 인기검색어
- 검색키워드
- 저자 : ( Ebenezer I. O. Ajayi ) (검색결과 2 건)
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Usman Abdulrasheed,Balogun Olayemi,Shuaib Bukhari Isah,Musa Bolanle O. P.,Yusuf Aminu Abba,Ajayi Ebenezer I. O. 대한감염학회 2023 Infection and Chemotherapy Vol.55 No.4
Background: Cytopenias serve as common indicators and crucial predictive tools for evaluating disease progression and therapeutic outcomes in individuals with human immunodeficiency virus (HIV) infection. This study aimed to assess the prevalence of cytopenias and their correlation with the level of immunosuppression in treatment-naive HIV-infected participants after initiating highly active combined antiretroviral drug therapy (cART24). Materials and Methods: This prospective study focused on evaluating cytopenia in 44 treatment-naive HIVinfected patients who consented to initiate cART and were consecutively enrolled. The research was conducted at the Nasara HIV Treatment & Care Centre of Ahmadu Bello University Teaching Hospital (ABUTH), Zaria, Nigeria, spanning from December 2016 to January 2018. Cytopenias, including anemia, leucopenia, lymphocytopenia, and thrombocytopenia, were defined and assessed according to World Health Organization guidelines. A combination of cross-sectional and longitudinal mixed-design two-step analysis was employed to validate our findings. Results: The median time from enrollment to cART initiation was 7 days, following the universal test and treat protocol. The prevalence of cytopenia was 75% at the baseline before treatment and increased to 84% after cART24 administration. There were no statistically significant differences in the median values of immuno-hematological parameters between baseline and after cART24 initiation (P >0.05). In terms of longitudinal assessment, the prevalence of anemia, leucopenia, lymphopenia, and thrombocytopenia at baseline were 66%, 23%, 0%, and 11%, respectively, and after cART24, the rates were 66%, 29%, 5%, and 20%. Notably, the prevalence of cytopenia correlated with declining CD4+ T cell counts. Among instances of unicytopenia, 58% exhibited isolated anemia, 6% had lone leucopenia, and 6% had solitary thrombocytopenia. Additionally, 27% demonstrated bi-cytopenia, and 3% exhibited pancytopenia. Interestingly, none of the study participants presented with lymphopenia. The most common combination was anemia and thrombocytopenia. Both longitudinal and cross-sectional analytical findings were consistent. Conclusion: In treatment-naive HIV-infected individuals, the prevalence of cytopenias, particularly anemia and thrombocytopenia, was substantial and correlated with the degree of immunosuppression as indicated by CD4+ T cell counts. These cytopenias persisted despite initiation of cART24, highlighting the complexity of hematological manifestations in HIV infection. Our study underscores the significant hematopathological impact of HIV and antiretroviral therapy, highlighting the necessity for preventive strategies to mitigate these adverse effects.
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( Pablo D. Cabral ),( Guillermo B. Silva ),( Sandra T. Baigorria ),( Luis I. Juncos ),( Ebenezer I. O. Ajayi ),( Néstor H. García ) 대한신장학회 2022 Kidney Research and Clinical Practice Vol.41 No.6
Background: Sodium chloride (NaCl) reabsorption in the cortical thick ascending limb (cTAL) is regulated by opposing effects. Nitric oxide (NO) inhibits NaCl reabsorption while 8-iso-prostaglandin-F2α (8-iso-PGF2α) stimulates it. Their interaction has not been evalu ated in the cTAL. Because 8-iso-PGF2α has considerable stability while NO is a free radical with a short half-life, we hypothesized that, in the cTAL, the inhibition of NaCl absorption will be reversed by 8-iso-PGF2α. Methods: Chloride absorption (J<sub>Cl</sub>) was measured in isolated perfused cTALs and whether the activation of protein kinase A (PKA) is required for this interaction. Since cyclic adenosine monophosphate (cAMP) is a major messenger for the 8-iso-PGF2α signaling cas cade, and NO inhibits J<sub>Cl</sub> by decreasing cAMP bioavailability, we measured 8-iso-PGF2α-stimulated cAMP in the presence of sodium nitroprusside (SNP). Results: The NO donor, SNP (10<sup>-6</sup> M), decreased J<sub>Cl</sub> by 41%, while luminal 8-iso-PGF2α (100 μM) increased J<sub>Cl</sub> to 315 ± 46 pmol/ min/mm (p < 0.003), reversing the effects of the NO donor. SNP inhibited J<sub>Cl</sub>, 8-iso-PGF2α failed to increase J<sub>Cl</sub> in the presence of H89. Basal cAMP was 56 ± 13 fmol/min/mm, in the presence of SNP 57 ± 6 fmol/min/mm, and 8-iso-PGF2α increased it to 92 ± 2 fmol/min/mm (p < 0.04). Conclusion: We concluded that 1) NO-induced inhibition of J<sub>Cl</sub> in the cTAL can be reversed by 8-iso-PGF2α, 2) 8-iso-PGF2α and NO in teraction requires PKA to control J<sub>Cl</sub>, and 3) in the presence of NO, 8-iso-PGF2α continues to stimulate J<sub>Cl</sub> because NO cannot reverse 8-iso-PGF2α-stimulated cAMP level.
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