Biomedical subjects

Sambor Grygorczuk

Publications and source records attributed to Sambor Grygorczuk.

39 records · Page 3Linked to original sources

PubMedDate not supplied

[Soluble CD40 and soluble CD40L concentrations in the serum and the cerebrospinal fluid of patients with tick borne encephalitis and neuroborreliosis].

BACKGROUND AND PURPOSE: The interaction between CD40 and CD40L is essential in generating of an immunological response also intrathecally. The aim of the study was estimation of a concentration soluble form of CD40, CD40L (CD154) in the bacterial and viral inflammation of the central nervous system in two compartments - blood circulation and intrathecally, before and after the treatment. MATERIAL AND METHODS: sCD40 and sCD40L were tested twice before and after treatment in pairs serum and CSF of 40 patients treated in the Dept. of Infectious Diseases and Neuroinfections. Patients were divided in two groups: (n=20) patients with tick borne encephalitis (TBE) (group I, n=20) and patients with neuroborreliosis in the form of lymphocytic meningitis (group II, n=20). ELISA assays were performed. RESULTS: Significantly increased concentrations of sCD40, sCD40L in CSF (higher in neuroborreliosis) were measured. We found also an increased concentration of sCD40L in inflammatory CSF in both tested groups (in neuroboreliosis lasting also after 4 weeks of treatment), compared with the control group (below the detection limit in normal CSF). CONCLUSIONS: Results of estimation of the sCD40 and sCD40L concentrations indicate their role in the intrathecal inflammation process of bacterial and viral etiology. The increased serum concentration of sCD40L in TBE and CD40 in neuroborreliosis indicate that peripheral activation of the immunological system persists after cessation of treatment and after the clinical recovery. The defense mechanisms are more pronounced in neuroborreliosis than in tick borne encephalitis.

Adult↗

PubMedDate not supplied

[Concentration of the beta-chemokine CCL5 (RANTES) in cerebrospinal fluid in patients with tick-borne encephalitis].

BACKGROUND AND PURPOSE: In tick-borne encephalitis (TBE), perivascular infiltrates are formed within the central nervous system (CNS) and are accompanied by pleocytosis with a predominance of T CD4+ lymphocytes in cerebrospinal fluid (CSF). Factors responsible for leukocyte flow into CNS in TBE have not been investigated. We evaluated the concentration of the chemotactic factor for lymphocytes, chemokine CCL5 (RANTES, Regulated upon Activation, Normal T cell Expressed and Secreted) in CSF and serum of patients with TBE and assessed its correlation with CSF pleocytosis. MATERIAL AND METHODS: Group I consisted of 10 patients with TBE virus infection presenting as meningitis; group II included 11 patients with TBE presenting as encephalomeningitis or myeloencephalomeningitis. The control group consisted of 8 patients, in whom neuroinfection and infection with TBE virus was excluded. The concentration of CCL5 was measured by ELISA in CSF and serum samples taken within 24 hours after hospitalization (examination 1) and in the convalescence period, on average after 16 days (examination 2). RESULTS: Mean CCL5 concentration in serum did not differ between the groups, while in CSF it was significantly increased in group I (64.3+/-75.5 pg/ml in examination 1 and 44.4+/-39.5 pg/ml in examination 2) and in group II (38.4+/-17.0 pg/ml in examination 1 and 48.8+/-24.7 pg/ml in examination 2) in comparison with controls (3.7+/-5.3 pg/ml). There was no significant difference regarding CCL5 concentration between groups I and II and between the examination 1 and 2. There was no correlation between the concentration of CCL5 and CSF parameters. CONCLUSIONS: The concentration of CCL5 is increased in CSF, but not in serum of patients with TBE. This increase does not depend on the clinical form of the disease and is sustained after the disappearance of the symptoms of acute infection. Further studies are necessary to determine the source of CCL5, and its role in the pathogenesis of TBE and its sequelae.

Adult↗

PubMedDate not supplied

[Post-lumbar puncture syndrome--its pathogenesis, prophylaxis and treatment].

Post-lumbar puncture syndrome (PLPS) is a frequent and important complication of diagnostic lumbar puncture. PLPS is primarily caused by perforation of the dura mater, leading to persistent leak of the cerebrospinal fluid, and, as a result, intracranial hypotension. Effective therapeutic options are limited to symptomatic treatment until natural improvement occurs, or, in cases of prolonged complaints, invasive treatment (epidural blood patch with patient's own venous blood), which makes prophylaxis of PLPS essential. Prophylactic measures of confirmed efficacy are: reducing needle size, positioning the needle bevel parallel to the long axis of the spine, re-inserting the stilet before withdrawal of the needle, and, if possible, using a so-called "atraumatic" needle, minimizing the perforation of the meninx. The volume of the cerebrospinal fluid collected and the position of the patient after the procedure do not have a significant influence on PLPS frequency.

Blood Patch, Epidural↗