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1.
Foot (Edinb) ; 46: 101693, 2021 Mar.
Article in English | MEDLINE | ID: mdl-33036837

ABSTRACT

BACKGROUND: Epidemiological data concerning the symptom 'foot drop' are scarce in the literature. However, everyday practice shows that this symptom is frequent, and that patients who suffer from it are significantly disabled. METHODS: A special 'foot-drop consulting hour' to examine and advise people with foot drop was founded. Over 18 months we collected data from 65 patients who consulted us: this included patient-related items, diagnoses and treatment. RESULTS: People of all ages were affected by foot drop. Left and right sides were affected with equal frequency. Spinal lumbar nerve root damage and peroneal nerve compression were the most frequent causes, followed by polyneuropathy and nerve trauma. In 18% of patients more than one pathological condition was found that might have led to foot drop. In 14% no reason could be determined. 45% of patients with foot drop subsequently received surgical treatment. CONCLUSION: Epidemiological data and details of patients affected by foot drop can help to raise awareness of this frequent symptom and to suggest specific therapy.


Subject(s)
Gait Disorders, Neurologic , Peroneal Neuropathies , Gait Disorders, Neurologic/diagnosis , Gait Disorders, Neurologic/epidemiology , Humans , Peroneal Nerve , Peroneal Neuropathies/diagnosis , Peroneal Neuropathies/epidemiology , Physical Examination
2.
Endocrine ; 10(3): 233-42, 1999 Jun.
Article in English | MEDLINE | ID: mdl-10484287

ABSTRACT

According to the oxidative hypothesis of atherosclerosis, a hyperoxidizability of lipoproteins could favor the development of the atherosclerotic process. Besides, it has been recently reported that models of elevated very-low-density-lipoprotein (VLDL) levels in rats resulted in an increased susceptibility of these VLDL to oxidation. Treatment with dexamethasone classically induces an increase in plasma VLDL concentration. The aim of our study was thus to assess the effects of a treatment with dexamethasone in rats on the susceptibility to copper oxidation, both on total plasma and on isolated lipoproteins. Male Sprague-Dawley rats aged three months were treated with a daily intraperitoneal injection of dexamethasone (1.5 mg per kg) for five days (DEX group), whereas control rats were fed ad libitum (AL group). In order to take into account the decrease of food intake induced by dexamethasone treatment, a group of pair-fed rats was constituted (PF group). These rats had the same food intake as rats of the DEX group and were treated with a daily isovolumic intraperitoneal injection of NaCl for 5 d. After 5 d treatment, rats were fasted overnight, then killed, and blood was collected on EDTA. Low-density lipoproteins (VLDL + LDL) and high-density lipoproteins (HDL) were isolated by ultracentrifugation. A copper oxidation was conducted both on total plasma and on isolated lipoproteins. As expected, after treatment with dexamethasone, plasma exhibited increased triglyceride and glucose levels. Similarly, VLDL + LDL of rats from the DEX group were enriched with triglycerides, when compared with VLDL + LDL of the other two groups of rats. Our major finding was a marked increase in the susceptibility of total plasma of the DEX group to copper oxidation, in comparison with the other two groups of rats. This oxidizability was assessed by the maximal level of oxidation products absorbing at 234 nm and classically considered to be conjugated dienes (7.46+/-0.70 micromol L(-1) in the DEX group vs. 3.36+/-0.40 and 2.05+/-0.60 micromol L(-1) in the AL and PF groups, respectively). Nevertheless, this higher oxidizability was not observed in the isolated lipoprotein fractions, as shown by the formation of lipid peroxidation products such as conjugated dienes, thiobarbituric-acid reactive substances, hydroperoxides, 7-ketocholesterol, and dienals. This is not in agreement with other models of hypertriglyceridemia that have been reported to induce a hyperoxidizability of lipoproteins in rats. Our results led us to hypothesize that other plasma components such as proteins could be involved in this susceptibility to oxidation. Indeed, the severe protein catabolism induced by dexamethasone treatment could support this hypothesis, by forming protein components that are more susceptible to oxidation, as shown by an increased carbonyl formation upon plasma copper oxidation.


Subject(s)
Copper Sulfate/pharmacology , Dexamethasone/pharmacology , Glucocorticoids/pharmacology , Lipid Peroxidation/drug effects , Lipoproteins/blood , Animals , Blood Glucose/metabolism , Lipoproteins, HDL/blood , Lipoproteins, LDL/blood , Lipoproteins, VLDL/blood , Male , Rats , Rats, Sprague-Dawley , Thiobarbituric Acid Reactive Substances/metabolism , Triglycerides/blood , Vitamin E/blood , beta Carotene/blood
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