New guidelines for the prevention of imported malaria in France.

Prevention of malaria is based on personal vector-control measures (PVCMs) to avoid mosquito bites at night and chemoprophylaxis if justified by the risk of contracting the disease. The most effective PVCM is the use of insecticide-treated mosquito nets. The decision to prescribe chemoprophylaxis, mainly to prevent Plasmodium falciparum infection, depends on the benefit-risk ratio. Overall, the risk of contracting malaria is 1,000-fold lower during a stay in the tropical regions of Asia or the Americas than in sub-Saharan Africa. For "conventional" stays (less than one month with nights spent in urban areas) in low-risk settings in tropical Asia and America, the risk of being infected with Plasmodium parasites (≤1/100,000) is equivalent or lower than that of experiencing serious adverse effects caused by chemoprophylaxis. Preventive medication is therefore no longer recommended. By contrast, in other settings and particularly in sub-Saharan Africa, chemoprophylaxis is the most effective measure against malaria. However, it is worth noting that no single preventive measure provides full protection. Regardless of the level of risk or chemoprophylaxis-related indication, protection against mosquito bites and rapid management of febrile illness after returning from an endemic area are also critical to prevent malaria. Finally, migrants of sub-Saharan origin visiting friends and relatives in their country of origin form a high-risk group who should be recommended chemoprophylaxis in the same way as any other travelers-with a preference for the least expensive molecules (doxycycline).

Mitochondrial complex I defect resulting from exercise-induced lower limb ischemia in patients with peripheral arterial disease.

This study aims to compare the structural and mitochondrial alterations between muscle segments affected by exercise-induced ischemia and segments of the same muscle without ischemia, in the same subject. In a prospective analysis, 34 patients presenting either peripheral arterial disease or chronic coronary syndrome without any evidence of peripheral arterial disease were eligible for inclusion based on findings indicating a need for either a femoro-popliteal bypass or a saphenous harvesting for coronary bypass. Before surgery, we assessed the level of exercise-induced ischemia in proximal and distal sections of the thigh by the measurement of transcutaneous oxygen pressure during an exercise treadmill test. Distal and proximal biopsies of the sartorius muscle were procured during vascular surgical procedures to assess mitochondrial function and morphometric parameters of the sartorius myofibers. Comparisons were made between the distal and proximal biopsies, with respect to these parameters. Thirteen of the study patients that initially presented with peripheral arterial disease had evidence of an isolated distal thigh exercise-induced ischemia, associated with a 35% decrease in the mitochondrial complex I enzymatic activity in the distal muscle biopsy. This defect was also associated with a decreased expression of the manganese superoxide dismutase enzyme and with alterations of the shapes of the myofibers. No functional or structural alterations were observed in the patients with coronary syndrome. We validated a specific model ischemia in peripheral arterial disease characterized by muscular alterations. This "Distal-Proximal-Sartorius Model" would be promising to explore the physiopathological consequences specific to chronic ischemia. NEW & NOTEWORTHY We compared proximal versus distal biopsies of the sartorius muscle in patients with superficial femoral artery stenosis or occlusion and proof of, distal only, regional blood flow impairment with exercise oximetry. We identified a decrease in the mitochondrial complex I enzymatic activity and antioxidant system impairment at the distal level only. We validate a model to explore the physiopathological consequences of chronic muscle ischemia.

[Impact of sickle cell trait on arterial stiffness in African subjects]. / Impact du trait drépanocytaire sur la rigidité artérielle des sujets africains.

Sickle cell trait (SCT) is the benign condition of sickle cell disease. Often asymptomatic, the carriers of the sickle cell trait have hemorheological disturbances with increased oxidative stress compared to healthy subjects. These disturbances can lead to structural and functional changes in large vessels. The aim of the study was to measure arterial stiffness, an independent marker of subclinical atherosclerosis, SCT carriers compared to sickle cell anemia (SCA) subjects. Nine SCT carriers aged 32±9 years (7 men) were compared to 14 SCA subjects aged 29±9 years (2 men) and 22 control subjects aged 34±9 years (11 men) recruited by the National blood transfusion center (CNTS) in Dakar (Senegal). Arterial stiffness was assessed by measurement of the finger-toe pulse wave velocity (PWVft) using pOpmètre® (Axelife SAS-France). The cardiovascular risk (CVR) was assessed according to the Framingham Laurier score. The SCT carriers had a higher PWVft (m/s) than SCA subjects (8.2±2.2 vs 6.1±0.9m/s, P=0.004) but not different from that of healthy controls (8.2±2.2 vs 7.4±1.8m/s, P=0.33). Linear regression showed a positive relationship between PWVft and the pulse pressure (PP) (P˂0.001; r2=0.39; F=13.20). The results show that the SCT carriers have stiffer arteries than SCA subjects. Linear regressions adjusted for age, mean arterial pressure (MAP) and PP, showed that only age and PP were independently correlated with arterial stiffness in the entire population.

Prevalence and Causes of Normal Exercise Oximetry in the Calf in Patients with Peripheral Artery Disease and Limiting Calf Claudication.

OBJECTIVE: In patients with claudication, an ankle brachial index (ABI) under 0.90 is considered to be abnormal and a sufficient argument for the arterial origin of exercise induced pain. Exercise transcutaneous oxygen pressure (Ex-tcpO2) can provide evidence of exercise induced regional blood flow impairment (RBFI) and confirm the arterial origin of walking induced pain. The frequency with which calf Ex-tcpO2 remains apparently normal in patients with claudication and abnormal ABI is unknown. Causes of these discrepant results have yet to be analysed. METHODS: A retrospective analysis of 4575 Ex-tcpO2 tests performed on 3,281 patients was conducted. The focus was on patients with a history of calf claudication and ABI under 0.90. Duplicate or non-standard tests were excluded, as were patients with no pain or those able to walk more than 15 minutes (on a treadmill). Searches were conducted for possible explanations of normal calf Ex-tcpO2 in the selected patients. RESULTS: Cardiorespiratory limitation was identified in 50 patients and isolated non-calf ischemia in 36 of the 106 patients selected. There was no obvious explanation during Ex-tcpO2, but clinical improvement after non-vascular treatment or total absence of improvement after a technically successful revascularisation was noted in 12 patients. Four patients were lost on follow up. Four patients improved after revascularisation, which suggests that the Ex-tcpO2 result was false negative. CONCLUSIONS: Ex-tcpO2 is negative in more than 20% of tests performed in patients with an ABI under 0.90 and a history of calf claudication. In most cases, when excluding re-tests and non-limiting or non-calf claudication on the treadmill, non-calf ischemia or a non-vascular limitation occurring during the test were observed. This observation supports both the value of treadmill testing in patients with calf claudication assumed to be of arterial origin (ABI<0.90) and the use of Ex-tcpO2 to detect non-calf ischemia.