Background:Guillain-Barré syndrome (GBS) is an acute inflammatory polyneuropathy commonly characterized by rapidly progressive, symmetric weakness and areflexia.Materials and Methods:We retrospectively assessed the clinical manifestations, results of electrodiagnostic tests, functional status and prognosis of 36 children diagnosed with GBS.Results:Based on clinical and electrophysiological findings, the patients were classified as having acute inflammatory demyelinating polyradiculoneuropathy (AIDP) (n = 25), acute motor axonal neuropathy (AMAN) (n = 10) and acute motor-sensory axonal neuropathy (AMSAN) (n = 1). Twenty (55.5%) patients were males and 16 (44.5%) patients were females. The mean age of the 36 patients was 68.1 ± 45.01 months (range, 6–180 months). Five (13.8%) patients were younger than 2 years. The most common initial symptoms were limb weakness, which was documented in 34 (94.4%) patients. In our study, 18 patients (51.4%) showed albuminocytological dissociation (raised protein concentration without pleocytosis) on cerebrospinal fluid (CSF) examination. Three patients (8.3%) required mechanical ventilation therapy during hospitalization. Unfortunately, three (8.3%) patients died; one patient had AIDP and two patients had axonal involvement (one case was AMAN and another case was AMSAN). When we compared the cases of residual sequel/dead and cases of complete recovery for neural involvement type including AIDP, AMAN and AMSAN, we did not find a statistically significant difference between the groups (P > 0.05).Conclusion:Our findings showed that cases of GBS was not uncommon in children younger than 2 years of age, and CSF protein level might be found high in the first week of the disease in about one half of the patients, with a higher rate of morbidity and mortality in patients with axonal involvement than in those with AIDP.
Trace elements are essential components of biological structures, but alternatively, they can be toxic at concentrations beyond those necessary for their biological functions. Changes in the concentration of essential trace elements and heavy metals may affect acute hemorrhagic stroke. The aim of this study was to measure serum levels of essential trace elements [iron (Fe), zinc (Zn), manganese (Mn), copper (Cu), and magnesium (Mg)] and heavy metals [cobalt (Co), cadmium (Cd), and lead (Pb)] in patients with acute hemorrhagic stroke. Twenty-six patients with acute hemorrhagic stroke and 29 healthy controls were enrolled. Atomic absorption spectrophotometry (UNICAM-929) was used to measure serum Fe, Cu, Pb, Cd, Zn, Co, Mn and Mg concentrations. Serum Cd, Pb and Fe levels were significantly higher in patients with acute hemorrhagic stroke than controls (p < 0.001), while serum Cu, Zn, Mg and Mn levels were significantly lower (all p < 0.001). However, there was no significant difference between the groups with respect to serum Co levels (p > 0.05). We first demonstrate increased Cd, Pb, and Fe levels; and decreased Cu, Zn, Mg, and Mn levels in patients with acute hemorrhagic stroke. These findings may have diagnostic and prognostic value for acute hemorrhagic stroke. Further studies are required to elucidate the roles of trace elements and heavy metals in patients with acute hemorrhagic stroke.
Previous studies have suggested that prolidase and nitric oxide (NO) regulate many processes, such as collagen synthesis and matrix remodeling. Oxidative stress plays an important role in the development of microvascular complications in diabetic patients. Data on serum prolidase activity in patients with diabetes mellitus or diabetic neuropathy (DN) are limited and conflicting. The aim of this study was to measure serum prolidase activity, NO, total antioxidant status (TAS), and malondialdehyde (MDA) levels in patients with DN. Forty-five patients with DN and 40 healthy controls were enrolled. Serum prolidase activity, TAS, MDA, and NO levels were determined. Serum MDA and NO levels were significantly higher in DN patients than controls (p = 0.002, p = 0.001, respectively), while prolidase activity and TAS levels were lower (p = 0.003, p = 0.001, respectively). Prolidase activity was negatively correlated with NO and MDA (r = -0.911, p < 0.001; r = -0.905, p < 0.001, respectively), while positively correlated with TAS (r = 0.981, p < 0.001) in DN patients. The current study is the first showing the decreased serum prolidase enzyme activity. Our results suggest that decreased collagen turnover may occur in DN patients, who have increased oxidative stress and increased NO levels. Decreased prolidase activity seems to be associated with increased NO levels and oxidative stress along with decreased antioxidant levels in DN. Therefore, decreased prolidase activity may play a role in pathogenesis of DN. Prospective clinical studies are necessary to confirm these findings.
This study indicates that PRES manifests predominantly with headache and visual impairment together. Adverse neonatal outcomes are also common in these patients.
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