Research Article
Frequency and Associated Factors of Hyperuricemia in a University Hospital in Dakar, Senegal
Pape Matar Kandji*
,
Ndeye Mareme Thioune,
Moustapha Djite,
Moustapha Ndep Sene,
Nene Oumou Kesso Barry,
Mariam El Idrissi,
Coumba Kamby,
Youssoupha Sene,
Abdou Fall,
Serigne Mbacke Mbow,
El Malick Ndour,
Fatou Gueye-Tall,
Papa Madieye Gueye
Issue:
Volume 14, Issue 3, September 2026
Pages:
66-71
Received:
28 July 2026
Accepted:
8 August 2026
Published:
27 August 2026
Abstract: Hyperuricemia is associated with gout, cardiovascular disease, chronic kidney disease, and metabolic disorders, yet data remain limited in Senegal. This study aimed to determine the frequency of hyperuricemia and its distribution according to age, sex, and clinical indication at Fann University Hospital. This retrospective observational study was conducted from January 1 to December 31, 2025, and included patients undergoing serum uric acid testing. Hyperuricemia was defined as serum uric acid > 70 mg/L in men, > 60 mg/L in women, and > 40 mg/L in children. Associated factors were assessed using logistic regression. A total of 2,023 patients were included. The mean age was 58.5 years, and the male-to-female ratio was 0.71. The overall frequency of hyperuricemia was 29.7% and was significantly higher in men than in women (33.3% vs. 27.1%; OR = 1.34; 95% CI: 1.10-1.62; P = 0.003). Hyperuricemia increased significantly with age (OR = 1.19; 95% CI: 1.12-1.26; P < 0.001). The highest frequencies were observed in patients evaluated for cardiovascular disease (40.0%), renal disease (38.5%), and arterial hypertension (32.3%). Nearly one-third of patients had hyperuricemia, with higher frequencies in men, older individuals, and patients with cardiorenal conditions. These findings highlight the relevance of serum uric acid testing in the biological assessment of at-risk patients.
Abstract: Hyperuricemia is associated with gout, cardiovascular disease, chronic kidney disease, and metabolic disorders, yet data remain limited in Senegal. This study aimed to determine the frequency of hyperuricemia and its distribution according to age, sex, and clinical indication at Fann University Hospital. This retrospective observational study was c...
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Research Article
Hemoglobin Variants Affect HPLC Measurement of HbA1c at Treichville University Hospital
Issue:
Volume 14, Issue 3, September 2026
Pages:
72-78
Received:
3 August 2026
Accepted:
12 August 2026
Published:
9 September 2026
Abstract: Hemoglobin A1c (HbA1c) measurement can be affected by hemoglobin variants through altered erythrocyte survival and method-specific analytical interference. This study assessed the influence of hemoglobin variants on HbA1c measurement by high-performance liquid chromatography (HPLC) in patients with hemoglobinopathy at Treichville University Hospital. This cross-sectional analytical study included 150 participants: 50 controls and 100 patients with confirmed hemoglobinopathy. Hemoglobin phenotypes were determined by electrophoresis. Blood glucose, complete blood count parameters, and the HPLC fractions HbA1c, HbA1a, HbA1b, and LA1C+ were measured. Group comparisons used the Mann-Whitney test, and phenotype comparisons used the Kruskal-Wallis test. The hemoglobinopathy group comprised SS (62%), SC (27%), AS (6%), an SFA2 electrophoretic profile (3%), and CC (2%). Mean blood glucose did not differ significantly between controls and participants with hemoglobinopathy (0.87 ± 0.13 g/L vs. 0.85 ± 0.07 g/L; p = 0.321). In contrast, mean HbA1c was markedly lower in the hemoglobinopathy group (1.29 ± 0.50% vs. 5.64 ± 0.54%; p < 0.001). Patients also had lower hemoglobin concentrations (8.75 ± 1.88 g/dL vs. 14.53 ± 1.58 g/dL; p < 0.001), indicating substantial anemia. HbA1c differed across electrophoretic categories (p = 0.0030), with the lowest values observed in CC and SFA2. LA1C+ also varied significantly by phenotype (p = 0.00011). Hemoglobin variants substantially affect HPLC HbA1c measurement and interpretation, producing a marked discordance between glycemia and HbA1c. In patients with hemoglobin variants, especially SS, SC, CC, or an SFA2 electrophoretic profile, HbA1c should not be interpreted in isolation and should be assessed alongside the chromatogram, blood glucose, hematological indices, and hemoglobin phenotype. Alternative glycemic markers may be required when HbA1c is unreliable.
Abstract: Hemoglobin A1c (HbA1c) measurement can be affected by hemoglobin variants through altered erythrocyte survival and method-specific analytical interference. This study assessed the influence of hemoglobin variants on HbA1c measurement by high-performance liquid chromatography (HPLC) in patients with hemoglobinopathy at Treichville University Hospita...
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Research Article
Kolaviron Attenuates Bifenthrin-INDUCED Cerebellar Neurotoxicity Through Multi-Target Modulation of
NF-κB/Nrf2/p38 MAPK Signaling
Ujong Peter Ujong,
Mbang Edet Ibor*,
Precious Takim Mgbe,
Edward Odey Emuru,
Runyi Bassey Ben,
Vivian Peter-Ujong
Issue:
Volume 14, Issue 3, September 2026
Pages:
79-88
Received:
18 August 2026
Accepted:
4 September 2026
Published:
28 September 2026
Abstract: Bifenthrin is a widely used type I pyrethroid insecticide whose exposure has been associated with neurotoxicity mediated by oxidative stress, inflammation, and apoptotic pathways. However, effective protective strategies against bifenthrin-induced cerebellar injury remain inadequately explored. This study investigated the protective effects of kolaviron against bifenthrin-induced cerebellar toxicity in rats and examined the possible involvement of oxidative, inflammatory, and apoptotic signaling pathways. Forty-eight rats were randomly assigned to six groups (n = 8): control, bifenthrin (1 mg/kg), kolaviron (200 mg/kg), kolaviron pretreatment (200 mg/kg) followed by bifenthrin (1 mg/kg), bifenthrin exposure followed by kolaviron post-treatment (200 mg/kg), and kolaviron co-treatment (200 mg/kg) with bifenthrin (1 mg/kg). Treatments were administered for 28 days. Oxidative stress markers, antioxidant enzymes, inflammatory mediators, apoptotic proteins, and relevant signaling molecules were evaluated alongside histopathological changes in the cerebellum. Bifenthrin exposure significantly decreased superoxide dismutase, catalase, glutathione, glutathione peroxidase, glutathione S-transferase, interleukin-4, and nuclear factor erythroid 2-related factor 2 (Nrf2), while significantly increasing malondialdehyde, tumor necrosis factor-α, interleukin-1β, cyclooxygenase-2, inducible nitric oxide synthase, caspase-3, p38 mitogen-activated protein kinase, and nuclear factor-κB (P < 0.05). Histological examination further revealed Purkinje cell degeneration and loss, vacuolation, and inflammatory cell infiltration. Kolaviron significantly ameliorated these biochemical, inflammatory, apoptotic, and histopathological alterations, with pretreatment producing the most consistent protective effects. conclusively, kolaviron attenuates bifenthrin-induced cerebellar toxicity by restoring redox homeostasis, enhancing Nrf2-associated antioxidant defense, and suppressing inflammatory and apoptotic signaling. Its protective activity may involve modulation of the Nrf 2/p38 MAPK/NF-κB signaling axis, resulting in the preservation of cerebellar architecture. These findings highlight kolaviron as a potential protective agent against bifenthrin-induced neurotoxicity.
Abstract: Bifenthrin is a widely used type I pyrethroid insecticide whose exposure has been associated with neurotoxicity mediated by oxidative stress, inflammation, and apoptotic pathways. However, effective protective strategies against bifenthrin-induced cerebellar injury remain inadequately explored. This study investigated the protective effects of kola...
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