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Toxoplasma encephalitis in HIV/AIDS patients in Prof. Dr. I.G.N.G. Ngoerah General Hospital, Bali, Indonesia Suryapraba, Anak Agung Ayu; Sintarani, Cokorda Istri Dyah; Vania, Aurelia; Ni Made Susilawathi; Anak Agung Raka Sudewi
Indonesian Journal of Biomedicine and Clinical Sciences Vol 56 No 4 (2024)
Publisher : Published by Universitas Gadjah Mada

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.22146/inajbcs.v56i4.16763

Toxoplasma gondii, an opportunistic infection in HIV/AIDS patients, is an obligate intracellular parasite that causes toxoplasma encephalitis (TE). The symptoms of TE range from subacute focal or global neurologic impairments to neuropsychiatric disorder, and infectious mass lesions. In clinical practice, presumptive diagnosis, including clinical syndrome, finding single or multiple brain lesions on neuroimaging evaluation are preferred. This study aimed to identify neurologic and radiologic characteristics of HIV/AIDS patients with TE in Prof. Dr. I.G.N.G Ngoerah Hospital, Denpasar, Bali. It was a retrospective study using medical records of patients with TE from January 2018 to December 2021. Of 122 subjects, 66.4% were male and 33.6% were female, age ranged from 19-59 y.o. with a median of age 33 y.o., and the CD4 count median was 29.5 cell/mm3. Decreased consciousness was the most prevalent clinical symptom in 40.2% of subjects followed by headache in 18.9% of subjects. A structural lesion in neuroimaging was primarily found in the basal ganglia area of the brain (44.3%). The fatality rate (30.3%) was significantly associated with decreased consciousness, higher leukocyte levels, and a higher neutrophil-to-lymphocyte ratio (p<0.05). Diagnosis of TE should be considered in immunocompromised young adults with subacute onset of focal and/or global neurological deficit and neuroimaging results showing hypodense lesion, particularly with ring-like enhancement, in thebasal ganglia and corticomedullary junction area of the brain. An altered state of consciousness and NLR can indicate poor outcomes in HIV/AIDS patients with TE.

Serum Nerve Growth Factor Levels in Painful Diabetic Neuropathy: A Systematic Review and Meta-Analysis Putu Indah Mahardika Putri; Ni Made Susilawathi; I Putu Eka Widyadharma
Bioscientia Medicina : Journal of Biomedicine and Translational Research Vol. 9 No. 12 (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.v9i12.1453

Background: Painful diabetic neuropathy (PDN) is a severe complication of type 2 diabetes mellitus (T2DM). Nerve Growth Factor (NGF) is vital for neuronal health, but its status as a systemic biomarker in PDN is contested due to conflicting reports on serum levels. This study aimed to quantitatively synthesize the literature on the association between serum NGF concentrations and the presence of PDN in patients with T2DM. Methods: PubMed, Scopus, Web of Science, and Embase were searched for observational studies from January 2015 to August 2025 that measured serum NGF in T2DM patients with PDN versus control groups (T2DM without PDN or healthy individuals). Data were independently extracted by two reviewers. A random-effects model was used to calculate the pooled Standardized Mean Difference (SMD) and 95% confidence intervals (CIs) to account for assay variability. Heterogeneity was explored using the I² statistic and meta-regression. Results: From 1,482 records, seven cross-sectional studies (485 PDN patients, 511 controls) were included. The meta-analysis revealed that patients with PDN had significantly lower serum NGF concentrations compared to controls, with a pooled SMD of -1.28 (95% CI: -1.79 to -0.77, p < 0.00001). Substantial heterogeneity was present (I² = 84%). Meta-regression showed that a longer duration of diabetes was significantly associated with a greater reduction in NGF levels (p = 0.02). No significant publication bias was detected. Conclusion: This meta-analysis provides consolidated evidence that lower systemic NGF levels are a strong feature of established PDN. The findings support the neurotrophic deficit hypothesis in PDN pathophysiology and identify NGF as a candidate biomarker requiring rigorous validation in longitudinal studies that carefully differentiate painful from painless neuropathy phenotypes.

Serum Nerve Growth Factor Levels in Painful Diabetic Neuropathy: A Systematic Review and Meta-Analysis Putu Indah Mahardika Putri; Ni Made Susilawathi; I Putu Eka Widyadharma
Bioscientia Medicina : Journal of Biomedicine and Translational Research Vol. 9 No. 12 (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.v9i12.1453

Background: Painful diabetic neuropathy (PDN) is a severe complication of type 2 diabetes mellitus (T2DM). Nerve Growth Factor (NGF) is vital for neuronal health, but its status as a systemic biomarker in PDN is contested due to conflicting reports on serum levels. This study aimed to quantitatively synthesize the literature on the association between serum NGF concentrations and the presence of PDN in patients with T2DM. Methods: PubMed, Scopus, Web of Science, and Embase were searched for observational studies from January 2015 to August 2025 that measured serum NGF in T2DM patients with PDN versus control groups (T2DM without PDN or healthy individuals). Data were independently extracted by two reviewers. A random-effects model was used to calculate the pooled Standardized Mean Difference (SMD) and 95% confidence intervals (CIs) to account for assay variability. Heterogeneity was explored using the I² statistic and meta-regression. Results: From 1,482 records, seven cross-sectional studies (485 PDN patients, 511 controls) were included. The meta-analysis revealed that patients with PDN had significantly lower serum NGF concentrations compared to controls, with a pooled SMD of -1.28 (95% CI: -1.79 to -0.77, p < 0.00001). Substantial heterogeneity was present (I² = 84%). Meta-regression showed that a longer duration of diabetes was significantly associated with a greater reduction in NGF levels (p = 0.02). No significant publication bias was detected. Conclusion: This meta-analysis provides consolidated evidence that lower systemic NGF levels are a strong feature of established PDN. The findings support the neurotrophic deficit hypothesis in PDN pathophysiology and identify NGF as a candidate biomarker requiring rigorous validation in longitudinal studies that carefully differentiate painful from painless neuropathy phenotypes.

A Neuroinflammatory Biomarker Profile Associated with Neuropathic Pain in Hansen's Disease: A Systematic Review and Meta-Analysis of S100B, TNF-α, and IL-6 Dian Rizki Fitria; I Putu Eka Widyadharma; Ni Made Susilawathi
Bioscientia Medicina : Journal of Biomedicine and Translational Research Vol. 10 No. 1 (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.v10i1.1475

Background: Neuropathic pain (NP) is a severe, chronic complication of Hansen's disease (HD), persisting after antimicrobial therapy and profoundly diminishing quality of life. Its pathophysiology is driven by persistent, complex neuroinflammatory processes within the peripheral nervous system. Circulating biomarkers, especially the glial-derived protein S100B, offer a potential objective window into this underlying pathology. This study aimed to meta-analyze the association between circulating S100B, TNF-α, and IL-6 and the presence of NP in patients with HD. Methods: A systematic search of PubMed, Scopus, and Web of Science databases was conducted for observational studies published between January 2015 and December 2025 that compared biomarker levels in HD patients with and without NP, diagnosed using validated screening instruments. Data from eligible studies were extracted independently, and methodological quality was assessed using the Newcastle-Ottawa Scale. A random-effects meta-analysis was performed to compute the pooled standardized mean difference (SMD) with 95% confidence intervals (CIs) for each biomarker. Results: Seven studies, comprising 812 patients (405 with NP, 407 without NP), met the inclusion criteria. The meta-analysis revealed that serum S100B levels were significantly elevated in HD patients with NP compared to those without (SMD = 1.28, 95% CI [0.95, 1.61], p < 0.001). This finding was accompanied by very high statistical heterogeneity (I² = 78%). Concurrently, the analysis demonstrated significantly higher circulating levels of TNF-α (SMD = 0.89, 95% CI [0.62, 1.16]) and IL-6 (SMD = 0.75, 95% CI [0.48, 1.02]) in the NP group. Conclusion: This meta-analysis establishes a strong statistical association between a distinct neuroinflammatory biomarker profile—characterized by elevated circulating S100B, TNF-α, and IL-6—and the presence of neuropathic pain in Hansen's disease. S100B, as a marker of Schwann cell distress, is a particularly relevant component of this profile. These findings underscore the pivotal role of neuroinflammation in HD-related NP, although the high heterogeneity and non-specific nature of these systemic markers necessitate a cautious interpretation regarding their immediate clinical applicability.

A Neuroinflammatory Biomarker Profile Associated with Neuropathic Pain in Hansen's Disease: A Systematic Review and Meta-Analysis of S100B, TNF-α, and IL-6 Dian Rizki Fitria; I Putu Eka Widyadharma; Ni Made Susilawathi
Bioscientia Medicina : Journal of Biomedicine and Translational Research Vol. 10 No. 1 (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.v10i1.1475

Background: Neuropathic pain (NP) is a severe, chronic complication of Hansen's disease (HD), persisting after antimicrobial therapy and profoundly diminishing quality of life. Its pathophysiology is driven by persistent, complex neuroinflammatory processes within the peripheral nervous system. Circulating biomarkers, especially the glial-derived protein S100B, offer a potential objective window into this underlying pathology. This study aimed to meta-analyze the association between circulating S100B, TNF-α, and IL-6 and the presence of NP in patients with HD. Methods: A systematic search of PubMed, Scopus, and Web of Science databases was conducted for observational studies published between January 2015 and December 2025 that compared biomarker levels in HD patients with and without NP, diagnosed using validated screening instruments. Data from eligible studies were extracted independently, and methodological quality was assessed using the Newcastle-Ottawa Scale. A random-effects meta-analysis was performed to compute the pooled standardized mean difference (SMD) with 95% confidence intervals (CIs) for each biomarker. Results: Seven studies, comprising 812 patients (405 with NP, 407 without NP), met the inclusion criteria. The meta-analysis revealed that serum S100B levels were significantly elevated in HD patients with NP compared to those without (SMD = 1.28, 95% CI [0.95, 1.61], p < 0.001). This finding was accompanied by very high statistical heterogeneity (I² = 78%). Concurrently, the analysis demonstrated significantly higher circulating levels of TNF-α (SMD = 0.89, 95% CI [0.62, 1.16]) and IL-6 (SMD = 0.75, 95% CI [0.48, 1.02]) in the NP group. Conclusion: This meta-analysis establishes a strong statistical association between a distinct neuroinflammatory biomarker profile—characterized by elevated circulating S100B, TNF-α, and IL-6—and the presence of neuropathic pain in Hansen's disease. S100B, as a marker of Schwann cell distress, is a particularly relevant component of this profile. These findings underscore the pivotal role of neuroinflammation in HD-related NP, although the high heterogeneity and non-specific nature of these systemic markers necessitate a cautious interpretation regarding their immediate clinical applicability.

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