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The Effect of KatG S315t M. Tuberculosis Gene Mutation on Conversion Rate of MDR-TB Patients with Shorter-Course Treatment Raden Ayu Linda Andriani; Zen Ahmad
Bioscientia Medicina : Journal of Biomedicine and Translational Research Vol. 4 No. 4 (2020): Bioscientia Medicina: Journal of Biomedicine and Translational Research
Publisher : HM Publisher

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.32539/bsm.v4i4.158

Abstract

Background. Resistance to the INH drug is most often caused by a mutation of the KatG S315T M.Tb gene. MDR TB treatment with short-term WHO mixes using high-dose INH drugs is considered less effective in this mutation condition because it causes high resistance to INH. The effectiveness of MDR TB treatment can be seen from the sputum smear conversion rate. This study was aimed to determine the effect of the S315T katG gene mutation on the treatment response of patients with MDR TB who received WHO short-term alloys at Dr Moh Hoesin general hospital, Palembang, Indonesia. Method. This study uses observational analytic with a prospective cohort approach. The study subjects were MDR TB patients at Dr Moh Hoesin general hospital, Palembang, Indonesia, and a PCR-RFLP examination was performed to see the katG gene, followed by sputum smear evaluation at the end of the first and second months of treatment to assess the speed of conversion. Data analysis using SPSS 25 with the chi-square statistical test. Results. The frequency of katG S315T M.Tb gene mutations was 51.85%. The majority of MDR TB sufferers experience rapid conversion (92.59%). 64.29% of the katG S315T gene mutation group experienced sputum smear conversion after one month, 28.57% after two months, and 7.14% after three months of treatment. There was no significant difference in conversion speed in the two groups (p = 0.741). Conclusion. There was no effect of the S315T M.Tb katG gene mutation on the speed of sputum smear conversion of MDR TB patients who received short-term alloy treatment.
The Effect of KatG S315t M. Tuberculosis Gene Mutation on Conversion Rate of MDR-TB Patients with Shorter-Course Treatment Raden Ayu Linda Andriani; Zen Ahmad
Bioscientia Medicina : Journal of Biomedicine and Translational Research Vol. 4 No. 4 (2020): Bioscientia Medicina: Journal of Biomedicine and Translational Research
Publisher : HM Publisher

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.32539/bsm.v4i4.158

Abstract

Background. Resistance to the INH drug is most often caused by a mutation of the KatG S315T M.Tb gene. MDR TB treatment with short-term WHO mixes using high-dose INH drugs is considered less effective in this mutation condition because it causes high resistance to INH. The effectiveness of MDR TB treatment can be seen from the sputum smear conversion rate. This study was aimed to determine the effect of the S315T katG gene mutation on the treatment response of patients with MDR TB who received WHO short-term alloys at Dr Moh Hoesin general hospital, Palembang, Indonesia. Method. This study uses observational analytic with a prospective cohort approach. The study subjects were MDR TB patients at Dr Moh Hoesin general hospital, Palembang, Indonesia, and a PCR-RFLP examination was performed to see the katG gene, followed by sputum smear evaluation at the end of the first and second months of treatment to assess the speed of conversion. Data analysis using SPSS 25 with the chi-square statistical test. Results. The frequency of katG S315T M.Tb gene mutations was 51.85%. The majority of MDR TB sufferers experience rapid conversion (92.59%). 64.29% of the katG S315T gene mutation group experienced sputum smear conversion after one month, 28.57% after two months, and 7.14% after three months of treatment. There was no significant difference in conversion speed in the two groups (p = 0.741). Conclusion. There was no effect of the S315T M.Tb katG gene mutation on the speed of sputum smear conversion of MDR TB patients who received short-term alloy treatment.
The Dual Role of Hypoxia-Inducible Factor-1α in Sepsis-Induced Immunomodulation and Organ Dysfunction: A Systematic Review and Meta-Analysis Hudari, Harun; Mega Permata; Ratna Maila Dewi Anggraini; Raden Ayu Linda Andriani
Bioscientia Medicina : Journal of Biomedicine and Translational Research Vol. 9 No. 9 (2025): Bioscientia Medicina: Journal of Biomedicine & Translational Research
Publisher : HM Publisher

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.37275/bsm.v9i9.1378

Abstract

Background: Sepsis, a life-threatening organ dysfunction caused by a dysregulated host response to infection, remains a leading cause of global mortality. Hypoxia-inducible factor-1α (HIF-1α) is a master transcriptional regulator of the cellular adaptive response to hypoxia but plays a complex, paradoxical role in sepsis. While essential for innate immune function, its sustained activation may amplify inflammation and drive organ damage. This meta-analysis was conducted to synthesize the evidence on the association of HIF-1α with key markers of immunomodulation and organ dysfunction in sepsis. Methods: We performed a systematic review and meta-analysis following PRISMA guidelines. A comprehensive search of PubMed, Scopus, and Web of Science was conducted for studies published between January 2014 and December 2024. We included observational studies that measured HIF-1α levels in adult sepsis patients and reported outcomes related to organ dysfunction (Sequential Organ Failure Assessment [SOFA] score) or mortality, and immunomodulation (Interleukin-6 [IL-6] levels). Seven studies meeting the inclusion criteria were included in the final analysis. Data were pooled using a random-effects model. Standardized Mean Difference (SMD) and Odds Ratios (OR) with 95% confidence intervals (CI) were calculated. Results: The seven included studies comprised 1,288 patients. The overall quality of the included studies was moderate to high as per the Newcastle-Ottawa Scale. The pooled analysis revealed that HIF-1α levels were significantly elevated in sepsis patients who died compared to those who survived (OR = 2.68, 95% CI: 1.55–4.64, p < 0.001), with moderate heterogeneity (I² = 45%). Furthermore, HIF-1α levels were strongly associated with greater organ dysfunction, as measured by the SOFA score (5 studies; SMD = 0.92, 95% CI: 0.51–1.33, p < 0.0001), with substantial heterogeneity (I² = 78%). HIF-1α levels also showed a significant positive correlation with the pro-inflammatory cytokine IL-6 (4 studies; SMD = 1.15, 95% CI: 0.65–1.65, p < 0.00001), with high heterogeneity (I² = 82%). Conclusion: This meta-analysis provides robust evidence that elevated HIF-1α levels are significantly associated with increased sepsis severity, characterized by greater organ dysfunction, a heightened pro-inflammatory state, and a higher risk of mortality. These findings underscore the maladaptive consequences of sustained HIF-1α activation in sepsis, positioning it as a critical prognostic biomarker and a complex, high-value target for future therapeutic modulation.
The Dual Role of Hypoxia-Inducible Factor-1α in Sepsis-Induced Immunomodulation and Organ Dysfunction: A Systematic Review and Meta-Analysis Hudari, Harun; Mega Permata; Ratna Maila Dewi Anggraini; Raden Ayu Linda Andriani
Bioscientia Medicina : Journal of Biomedicine and Translational Research Vol. 9 No. 9 (2025): Bioscientia Medicina: Journal of Biomedicine & Translational Research
Publisher : HM Publisher

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.37275/bsm.v9i9.1378

Abstract

Background: Sepsis, a life-threatening organ dysfunction caused by a dysregulated host response to infection, remains a leading cause of global mortality. Hypoxia-inducible factor-1α (HIF-1α) is a master transcriptional regulator of the cellular adaptive response to hypoxia but plays a complex, paradoxical role in sepsis. While essential for innate immune function, its sustained activation may amplify inflammation and drive organ damage. This meta-analysis was conducted to synthesize the evidence on the association of HIF-1α with key markers of immunomodulation and organ dysfunction in sepsis. Methods: We performed a systematic review and meta-analysis following PRISMA guidelines. A comprehensive search of PubMed, Scopus, and Web of Science was conducted for studies published between January 2014 and December 2024. We included observational studies that measured HIF-1α levels in adult sepsis patients and reported outcomes related to organ dysfunction (Sequential Organ Failure Assessment [SOFA] score) or mortality, and immunomodulation (Interleukin-6 [IL-6] levels). Seven studies meeting the inclusion criteria were included in the final analysis. Data were pooled using a random-effects model. Standardized Mean Difference (SMD) and Odds Ratios (OR) with 95% confidence intervals (CI) were calculated. Results: The seven included studies comprised 1,288 patients. The overall quality of the included studies was moderate to high as per the Newcastle-Ottawa Scale. The pooled analysis revealed that HIF-1α levels were significantly elevated in sepsis patients who died compared to those who survived (OR = 2.68, 95% CI: 1.55–4.64, p < 0.001), with moderate heterogeneity (I² = 45%). Furthermore, HIF-1α levels were strongly associated with greater organ dysfunction, as measured by the SOFA score (5 studies; SMD = 0.92, 95% CI: 0.51–1.33, p < 0.0001), with substantial heterogeneity (I² = 78%). HIF-1α levels also showed a significant positive correlation with the pro-inflammatory cytokine IL-6 (4 studies; SMD = 1.15, 95% CI: 0.65–1.65, p < 0.00001), with high heterogeneity (I² = 82%). Conclusion: This meta-analysis provides robust evidence that elevated HIF-1α levels are significantly associated with increased sepsis severity, characterized by greater organ dysfunction, a heightened pro-inflammatory state, and a higher risk of mortality. These findings underscore the maladaptive consequences of sustained HIF-1α activation in sepsis, positioning it as a critical prognostic biomarker and a complex, high-value target for future therapeutic modulation.