Date

6-2015

Document Type

Thesis

Degree Name

M.P.H.

Department

Dept. of Public Health & Preventive Medicine

Institution

Oregon Health & Science University

Abstract

Objective

To determine whether the odds of having konzo, a tropical spastic paraparesis associated with food (cassava) cyanogenic exposure, were associated with lower cyanide detoxification rates (CDR) and malnutrition.

Study Design And Setting

A case-control study was conducted in the rural district of Kahemba, Democratic Republic of Congo.

Methods

One hundred and twenty-two children (5 to 17 year-old) with konzo as per the WHO criteria for the disease were age and sex-matched with 87 presumably healthy controls. Exposure to cassava cyanogens was ascertained by measuring the concentrations of thiocyanate (SCN) in plasma (P-SCN) and urines (U-SCN). Children with Height-for- Age z-score < - 2 were classified as stunted. CDR was measured as rhodanese enzyme activity expressed in milliseconds required to detoxify cyanide and yield one μmole of SCN per mg of protein [ms/(μmol/mg protein)] or, alternatively, the amount of SCN in millimoles produced per minute in one ml of plasma [mmolSCN/(ml plasma/min)] during the cyanide detoxification process. Data were analyzed using conditional regression models with the significance level set at 0.05.

Results

The mean (SD) U-SCN concentration in children with konzo was 522.3 (354.3) μmol/l, significantly higher than the 384.6 (223.7) μmol/l concentration in those without konzo (P < 0.05). The disease was associated with stunting (OR: 5.8; 95% CI: 2.7 – 12.8; p < 0.01; N= 83 paired groups) and higher U-SCN concentration (OR: 1.1; 95% CI: 1 – 1.20 per 50-μmol increase in U-SCN; p < 0.03; N = 47 paired groups). CDR appeared slower in children with konzo [mean (SD) CDR: 427.1 (217.8) ms/(μmol/mg protein) or, equivalently, 11.5 (4.5) mmol SCN/(ml plasma/min)] compared to those without konzo [410.4 (175.9) ms/(μmol/mg protein) or 12.5 (5.4) mmol SCN/(ml plasma/min)]. After adjusting for stunting and U-SCN concentration, the odds of developing konzo was reduced by 63% (95% CI: 11 – 85%, p = 0.03; N = 41 paired groups) for each 5 mmol SCN/(ml plasma/min)-increase in the CDR.

Conclusion

Poor cyanide detoxification combined with higher U-SCN concentrations in children with konzo suggest that they may be experiencing a higher exposure to cassava cyanogens relative to those without konzo. Children with konzo appear to be at risk for recurrent toxic injuries. Prevention of the disease may require both a safer processing of cassava prior to human consumption and strategies to enhance the human detoxification process of cyanide in those relying on cyanogenic cassava as the main source of food. Nutritional rehabilitation must be key to the prevention of the cassava related neurological diseases.

Identifier

doi:10.6083/M4CV4GGF

School

School of Medicine

Available for download on Sunday, June 17, 2018

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