Full blood counts, ESR, CRP, haematinics and markers for oxidative stress were measured for 33 patients diagnosed with chronic fatigue syndrome (CFS) and 27 age and sex matched controls. All participants also completed symptom questionnaires. CFS patients had increases in malondialdehyde (P <0.006), methaemoglobin (P <0.02), mean erythrocyte volume (P <0.02) and 2,3-diphosphoglycerate (P <0.04) compared with controls. Multiple regression analysis found methaemoglobin to be the principal component that differentiated between CFS patients and control subjects. Methaemoglobin was found to be the major component associated with variation in symptom expression in CFS patients (R(2) = 0.99, P <0.00001), which included fatigue, musculoskeletal symptoms, pain and sleep disturbance. Variation in levels of malondialdehyde and 2,3-diphosphoglycerate were associated with variations in cognitive symptoms and sleep disturbance (R(2) = 0.99, P <0.00001). These data suggest that oxidative stress due to excess free radical formation is a contributor to the pathology of CFS and was associated with symptom presentation.

BackgroundIn Nigeria, reports on the prevalence of modifiable cardiovascular disease (CVD) risk factors are scarce. In addition, socio-economic status (SES), an important component of the socioeconomic gradient in CVD and its risk factors has not been clearly elucidated. This study sought to assess the prevalence of CVD risk factors and how the difference in prevalence and accessibility to CVD risk screening across income levels and educational backgrounds contributes to disease diagnosis in rural and urban Nigerian adults.MethodsA cross sectional study was carried out on a sociocultural ethnic group of persons living in rural and urban settings. All participants were aged ≥ 18 years. The WHO STEPS questionnaire was used to document the demographics, history of previous medical check-up or screening, anthropometric and biochemical measurements of the participants. Average income level and educational status were indicators used to assess the impact of SES. Multivariate analyses were performed to assess any difference between the geographical locations and SES indicators, and prevalence of CVD risk factors and access to CVD risk screening.ResultsThe 422 participants (149 males and 273 females) had mean age (± standard deviation) of 38.3 ± 20.5 and 42.9 ± 20.7 years, respectively. Only total cholesterol (p = 0.001), triglyceride (p = 0.005), high density lipoprotein cholesterol (HDL) (p < 0.0001), body mass index (BMI) (p = 0.03) and average income rate (p = 0.01) showed significant difference between gender groups. Overall prevalence of prediabetes (4.9%), diabetes (5.4%), hypertension (35.7%), low HDL (17.8%), hypertriglyceridemia (23.2%), hypercholesterolemia (38.1%) and central obesity of 52.2% was recorded. Except between total cholesterol (p = 0.042) and HDL (p = 0.017), other CVD risk factors did not show a statistical significance across income levels. Participants with ‘university and postgraduate education’ had higher access to blood pressure and blood glucose screening compared to other educational groups; and this showed a statistical significance.ConclusionThis study has shown that a significant number of modifiable CVD risk factors exist in the rural and urban migrants of an adult Nigerian population. While income level did not affect the CVD risk factor prevalence, it did affect accessibility to CVD risk screening. There is a need for access to diagnosis of modifiable risk factors at all levels of society.

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Thrombotic microangiopathy (TMA) is a term used to describe a group of disorders characterized by hemolytic anemia (with prominent red blood cell fragmentation), thrombocytopenia, and thrombosis in the microvasculature. It may be used when describing patients with thrombotic thrombocytopenic purpura (TTP), hemolytic uremic syndrome, atypical hemolytic uremic syndrome, as well as a myriad of other disorders in which the TMA may be secondary to another disease or disorder. While limited information exists as to the exact cause of microthrombosis in many TMA, recent advances have been made in the understanding of TTP and its pathophysiology. This progress can be attributed to discovery of the von Willebrand factor cleaving protease ADAMTS-13 (a disintegrin and metalloproteinase with a thrombospondin type 1 motif, member 13), whose absence in TTP has given the disorder a distinct molecular identity. The discovery of this metalloprotease has prompted a significant amount of research relating to its role in TTP as well as its general function in hemostasis. The exact mechanisms by which this metalloprotease achieves its role are slowly being understood and these now provide other avenues by which TMA may occur.

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