Traditional Foods as Putative Sources of Antioxidants with Health Benefits in Konzo

Konzo is a toxico-nutritional neurological disease associated with oxidative damage induced by cyanide poisoning through the ingestion of poorly processed bitter cassava. Dietary uses and patterns, determined using food frequency questionnaires, structured interviews and direct observation in consenting households to Kahemba, the rural area most affected by konzo in the world, showed that the diet of affected population is not varied and largely dependent on cassava (Manihot esculenta Crantz) products. Commonly consumed foodstuffs include herbal teas, mushrooms, spices, vegetables and yams. Phytochemical composition of extracts revealed that they contained flavonoids and phenolic acids as major compounds. All extracts of investigated traditional foods at the concentration range of 0.25–20 μg/mL, displayed high radical scavenging and cellular antioxidant activities using lucigenin on equine neutrophils, related to their phenolic content. The leaves of Manihot esculenta and Manihot glaziovii exhibited the highest antioxidant activity among vegetables. Lippia multiflora is the most active of the herbal teas, Auricularia delicata of mushrooms, Dioscorea alata of yams and Ocimum basilicum of spices. Traditional foods showed more efficient effects on extracellular ROS production and MPO activity. Traditional foods have interesting antioxidant, anti-inflammatory properties and could putatively be used as functional foods or nutraceuticals in the prevention of oxidative damage associated with konzo

Indice global des signes neurologiques du konzo: marqueur clinique de multiples facteurs de susceptibilite et de gravite des troubles neurocognitifs chez l’enfant en milieu Konzo

Objectif : Quantifier la détérioration neurologique observée dans le konzo eu égard aux multiples déficiences incriminées dans sa pathogénie. Méthodes : Une étude transversale a été entreprise auprès de 123 enfants konzo et 87 non-konzo (4-17 ans) en 2011 à Kahemba, Congo-Kinshasa. L’indice global de signes neurologiques du konzo (IGSNK) était étudié en relation avec le niveau socio-économique familial évalué par le HOME, les performances cognitives au KABC-II et motrices au BOT-2, les taux sériques des isoprostanes, oligoéléments, et l’albuminémie et triglyceridémie mesurés respectivement par LC-MS/MS, ICP-MS, et automate Piccolo. Les tests de χ2, de Mann-Whitney et Kruskal-Wallis, ou la corrélation r de Spearman ont été appliqués au seuil de signification de 0,05. Résultats : L’augmentation de l’indice global des signes neurologiques du konzo était associée à la sévérité de la maladie (p < 0,001), le niveau socioéconomique familial (r = – 0,25 ; p < 0,001, la triglyceridémie (r = 0,55 , p = 0,001) et les 8,12-IsoProstaneF2-VI sériques (r = 0,33 , p= 0,06),), l’albuminémie (r = – 0,44 , p = 0,010 ) , la cuprémie ( r = – 0,36 , p= 0,048), le sélenium sérique (r = – 0,57, p = 0,001) ; en plus de l’habilité motrice globale (r = -0,861 ; p < 0,001) et l’indice global de fonctionnement cognitif (r = – 0,44 ; p = 0,002).Conclusion : L’indice global des signes neurologiques du konzo paraît être un bon marqueur clinique de multiples déficiences (pauvreté socio-familiale, malnutrition, stress oxydatif) incriminées dans la sévérité du konzo.Mots clés: malnutrition, niveau socio-économique familial, stress oxydatif, konzo, intoxication cyanhydrique, troubles moteurs et cognitifs  Konzo global neurological index: a clinical marker of susceptibility and severity of neurocognitive deficits in children living in Konzo-affected areasObjective: To quantify the extent of neurological deficits in konzo in a context of multiple factors incriminated in its pathogenesis. Methods: A cross-sectional study was carried out to assess 123 children with and 87 presumably healthy controls (4-17 years) in 2011 in kahemba, congo-kinshasa. A konzo global neurological index (KGNI) was constructed and assessed in relation to socio-economic status (assessed using the home questionnaire),  cognitive and motor performances at the KABC-II and BOT-2, respectively; serum isoprostanes (measured by LC/MS-MS), trace elements (by ICP-MS), albumin and triglycerides (by automated Piccolo). The chi-square, Mann-Whitney and Kruskal-Wallis tests as well as the Spearman r coefficients were used at the 0.05 level of statistical significance.Results: A higher KGNI was significantly associated with the severity of konzo (p < 0.001), poor socio-economic status (r = – 0.25, p < 0.001), elevated serum triglycerides (r = 0.55, p = 0.001), 8,12-isoprostane F2-VI (r = 0.33, p = 0.06), hypoalbuminemia (r = – 0.44, p = 0.010), low serum concentrations copper (r = – 0.36, p = 0.048) or selenium (r = – 0.57, p = 0.001);in addition to poor scores at the BOT-2 testing (r = -0.86; p < 0.001) and KABC-II testing for cognition (r = – 0.44; p = 0.002).Conclusion: The konzo global neurological index appears to be a good clinical marker of disease susceptibility factors (poor socio-economic status, malnutrition, oxidative stress) incriminated in the severity of konzo.Key words: malnutrition, socio-economic status, oxidative stress, cyanide intoxication, neurocognitio

Troubles socio-émotionnels de l’enfant en milieu Konzo, un syndrome paralytique de nature épidémique associé à une intoxication cyanhydrique d’origine alimentaire en Afrique sub-saharienne

Introduction: l’objectif de cette étude était d’élucider le profil socio-émotionnel de l’enfant en milieu Konzo, une paralysie toxico-nutritionnelle sévissant en Afrique sub-saharienne. Méthodes: nous avons évalué le profil socio-émotionnel de 210 enfants dont 123 avec konzo et 87 présumés contrôles sains (4-17 ans d’âge) après interview structuré avec les parents lors d’une enquête épidémio-clinique du konzo en 2011 au Congo-Kinshasa. Le profil neurocognitif était documenté par le KABC-II, le BOT-2 et l’indice global des signes neurologiques du Konzo (IGSNK). Les tests associatifs ont été réalisés par le test de Chi-carré, la régression logistique, dans le cas échéant par modèle linéaire généralisé, au seuil de signification de 0,05. Résultats: dans l’ensemble, l’irritabilité, la violence physique ou l’inhibition avec ou sans tristesse étaient respectivement retrouvés dans 46,0%, 30,2%, 18,7%; avec un risque accru pour le Konzo (OR = 2,6; IC95%: 1,4 - 4,8; p = 0,001). Le trouble socio-émotionnel était associé à l’insuffisance pondérale (OR: 0,49; IC95%: 0,31 - 0,78; p = 0,002) et à un IGSNK élevé (OR: 1,33; IC 95%: 1,1-1,63; p=0,019); et par ailleurs aggravait les déficits cognitifs dans le Konzo (interaction statut neurologique χ troubles socio-émotionnels, D = 6,297; p = 0,013). Des performances cognitives élevées étaient observées chez les enfants non-Konzo mais avec troubles socio-émotionnels. La concentration moyenne (écart-type ± ET) de thiocyanate urinaire était plus élevé (554,8 ± 371,6 µmol/l) chez les enfants Konzo avec troubles socio-émotionnels. Conclusion: l’enfant vivant en milieu Konzo présente des troubles socio-émotionnels. Leur nature psychopathologique et l’impact sur la cognition nécessitent des études approfondies

Frequency by severity grade in the 781 study subjects.

<p>Frequency by severity grade in the 781 study subjects.</p

Syndromic and functional aspects of clinical presentation in the 781 study subjects.

<p>Syndromic and functional aspects of clinical presentation in the 781 study subjects.</p

Unadjusted odds of death.

<p>Unadjusted odds of death.</p

Mortality trends and risk factors in advanced stage-2 Human African Trypanosomiasis: A critical appraisal of 23 years of experience in the Democratic Republic of Congo

<div><p>We conducted a retrospective study on mortality trends and risk factors in 781 naïve cases of advanced stage-2 sleeping sickness admitted between 1989 and 2012 at the National Reference Center for Human African Trypanosomiasis (HAT), Department of Neurology, Kinshasa University, Democratic Republic of Congo (DRC). Death was the outcome variable whereas age, gender, duration of disease, location of trypanosomes in body fluids, cytorachy, protidorachy, clinical status (assessed on a syndromic and functional basis) on admission, and treatment regimen were predictors in logistic regression models run at the 0.05 significance level. Death proportions were 17.2% in the standard melarsoprol schedule (3-series of intravenous melarsoprol on 3 successive days at 3.6 mg/kg/d, with a one-week interval between the series, ARS 9); 12.1% in the short schedule melarsoprol (10 consecutive days of intravenous melarsoprol at 2.2 mg/kg/d, ARS 10), 5.4% in the first-line eflornithine (14 days of eflornithine at 400 mg/kg/d in 4 infusions a day DFMO B), 9.1% in the NECT treatment regimen (eflornithine for 7 days at 400, mg/kg/d in 2 infusions a day combined with oral nifurtimox for 10 days at 15 mg/kg/d in 3 doses a day); and high (36%) in the group with select severely affected patients given eflornithine because of their clinical status on admission, at the time when this expensive drug was kept for treatment of relapses (14 days at 400 mg/kg/d in 4 infusions a day, DFMO A). After adjusting for treatment, death odds ratios were as follows: <b>10.40</b> [(95% CI: 6.55–16.51); p = .000] for clinical dysfunction (severely impaired clinical status) on admission, <b>2.14</b> [(95% CI: 1.35–3.39); p = .001] for high protidorachy, <b>1.99</b> [(95% CI: 1.18–3.37); p = .010] for the presence of parasites in the CSF and <b>1.70</b> [(95% CI: 1.03–2.81); p = .038] for high cytorachy. A multivariable analysis within treatment groups retained clinical status on admission (in ARS 9, ARS 10 and DFMO B groups) and high protidorachy (in ARS 10 and DFMO B groups) as significant predictors of death. The algorithm for initial clinical status assessment used in the present study may serve as the basis for further development of standardized assessment tools relevant to the clinical management of HAT and information exchange in epidemiological reports.</p></div

Proportion of deaths by clinical status on admission by treatment.

<p>Black bar = deceased, dysfunctional on admission; dashed bar = deceased, non-dysfunctional on admission.</p

Yearly distribution of deaths and severely affected subjects on admission over the study period.

<p>Plain line = number of deaths per year; dotted line = number of severe (dysfunctional) cases on admission per year.</p

Stage-2 HAT severity assessment chart.

<p>Stage-2 HAT severity assessment chart.</p