[Antibodies to ganglioside GM1 and Campylobacter jejuni in patients with Guillain-Barré syndrome].

Guillain-Barré syndrome (GBS) is an acute immune mediated neuropathy, polyradiculoneuritis, characterized by rapid onset of symmetric extremity muscle paralysis, areflexia and albuminocytological dissociation in the cerebrospinal fluid (CSF). Recently, the heterogeneity of GBS has been noticed with definition of several GBS variants. The axonal GBS associated with anti-GM1 antibodies is the most important variant with the specific role of Campylobacterjejuni (CJ) in the induction of the disease. The role of our study was to determine the frequency of antecedent infection with CJ in the population of our patients with GBS, the association with anti-GM1 antibodies and the distribution of these antibodies within clinical forms of the disease. The diagnosis of GBS has been established in 17 patients according to clinical, electrophysiological and laboratory (CSF) criteria. The serum antibodies to 63 kDa flagellar protein isolated from CJ serotype 0:19 were determined by ELISA and Western blot and serum anti-GM1 antibodies by ELISA. In relation to the disability score two patients were ambulatory, five were ambulatory with support, seven were bedridden and two patients needed respirator. Five (29%) patients had pure motor, while 12 (71%) had sensorimotor GBS. The cranial nerves were involved in 11 (65%) and 9 (53%) patients had autonomic dysfunction. Electromyoneurography showed primary axonal, predominantly motor neuropathy in 6 (35%) and demyelinating sensorimotor neuropathy in 11 (65%) patients. The CSF protein content ranged from 0.47 to 3.88 g/L. The antecedent infection with CJ was shown by serum antibodies to CJ flagellar protein in 12 (71%) patients. Fifteen (88%) patients had IgG anti-GM1 antibodies. Twelve (71%) patients had both antibodies. In relation to the clinical form, anti-CJ antibodies were found in 8 (73%) out of 11 patients with demyelinating GBS and in 4 (66.6%) out of 6 patients with axonal GBS. The high titer of anti-GM1 antibodies was found in all patients (100%) with axonal and in 9 (82%) out of 11 patients with demyelinating GBS. The association of IgG anti-CJ and IgG anti-GM1 antibodies was found in 4 (66.6%) out of 6 patients with axonal and in 8 (73%) out of 11 patients with demyelinating GBS. The main features of our patients with GBS were high frequency of antecedent infection with CJ, unusually frequent association with anti-GM1 antibodies, and equally frequent association of anti-CJ and anti-GM1 antibodies in both, axonal and demyelinating GBS.

[Helicobacter pylori--clinical manifestations, diagnosis and therapy].

During the past 20 years the role of Helicobacter pylori have been topic of intensive research. Studies have established that H. pylori can cause acute and chronic gastritis, duodenitis, gastric peptic ulcers and duodenal ulcers non-ulcer dyspepsia and Weird diseases and syndroms. H. pylori has been identified as a risk factor for gastric cancer and MALT-lymphoma. Nearly more than 90% of patients with duodenal ulcus, more than 70% of those with gastric ulcer and more than 80% patients with the gastric cancer have H. pylori infection. The discovery of the infective nature of peptic diseases and involvement of of H. pylori in theirs aetiology has begin to change our views on haw to approach diagnosis and therapeutic treatment in the practice. For this aim have been developed several methods which can be used to diagnose of H. pylori: invasive as endoscopy and non-invasive such as urea-breath-test, detection of antigens in stool, detection of specific antibodies in patients sera by means of serological tests--ELISA and Immunblott, molecular tests PCR and fluorescence-in situ- hybridisation for the detection of H. pylori and its resistance for clarithromycine and metronidazole. There are several effective treatments which can cure gastric and duodenal ulcers as well as prevent theirs recurrences.