Fetal-maternal incompatibility in the Rh system. Rh isoimmunization associated with hereditary spherocytosis: case presentation and review of the literature.

Next to A and B antigens, agglutinogen D exhibits the highest immunogenicity. Following the transfusion of D-positive red blood cells (RBCs), almost 80% of D-negative recipients develop anti-D antibodies (Abs). Subsequently, anti-D immunization further promotes the synthesis of Abs towards other blood group antigens in or outside the Rh system. The D antigen is also involved in 95% of cases of hemolytic disease of the newborn. Transfusions, hemotherapy, grafts, and obstetric history (abortions, ectopic pregnancy, births) are all risk factors for Rh isoimmunization. In the case of ABO compatibility between mother and fetus, Rh-positive fetal RBCs that have reached the maternal bloodstream are not destroyed by group agglutinins, and Rh antigenic sites are not hidden by the maternal immune system. But a Rh-negative mother with a homozygous Rh-positive husband will certainly have a Rh-positive fetus. As it has an irreversible evolution, the Rh isoimmunization once installed cannot be influenced in the sense of decreasing the Ab titer, therefore, injectable globulin has no effect. A particular case was that of a newborn with Rh system incompatibility associated with hereditary spherocytosis The clinical balance at birth reflects the severe jaundice of the female newborn of 3140 g, gestational age 38∕39 weeks, extracted by lower-segment transverse Caesarean section, with a double loop nuchal cord, Apgar score 8. Because the jaundice was severe and atypical (face and upper chest), we considered the possibility of coexistence of hemolytic disease of the newborn by Rh blood group incompatibility associated with hereditary spherocytosis, as it turned out to be true and mentioned. Changes in genes encoding proteins in the structure of the RBC membrane have amplified hemolysis induced by maternal-fetal isoimmunization in the Rh system. Massive hemolysis accentuated by congenital spherocytosis, confirmed later, imposed blood transfusion and dynamic monitoring.

The Analysis of Blood Inflammation Markers as Prognostic Factors in Parkinson's Disease.

Parkinson's disease is a chronic, progressive, and neurodegenerative disease, and yet with an imprecise etiopathogenesis. Although neuroinflammation was initially thought to be a secondary condition, it is now believed that microglia-induced inflammation could also contribute to the degeneration of the nigrostriatal pathway. Here, we aimed to establish the feasibility of basic inflammatory biomarkers as prognostic factors in PD. The study was based on retrospective analyses of blood samples taken from patients diagnosed with PD, as well as from healthy subjects. Complete medical records, total leukocyte count with subpopulations, and erythrocyte sedimentation rate (ESR) were analyzed. We calculated the serum neutrophils-to-lymphocytes ratio (NLR) and platelet-to lymphocytes ratio (PLR), and also compared the laboratory data between the PD group and the control group. Only PLR and NLR showed statistically significant differences (p < 0.001 and 0.04, respectively). In our study, ESR did not show statistically significant correlations with motor score or with disability. In our research, ESR was correlated with the disease duration (p = 0.04), and PLR showed a significant correlation with disease stage (p = 0.027) and disease duration (p = 0.001), but not with motor state. These biomarkers could prove to be effective tools for a primary evaluation of inflammation in PD, but further tests are required to properly investigate the neuroinflammatory status of these patients.

A case of tuberculous meningitis and the role of perivascular spaces in lymph cell migration in the brain.

Meningitis and encephalitis are inflammatory diseases in which acute and chronic inflammatory cells infiltrate leptomeninges, especially the arachnoid, and migrate through the subarachnoid space and by diapedesis, in order to extend around blood vessels and into the brain parenchyma. To what extent migrated/resident inflammatory cells participate to these interactions, or what are exactly the initial steps by which these cells reach the brain interstitium, it is not yet completely known. Recent years have brought new insights into the description of water flow circuits in the brain, suggesting that the cerebrospinal fluid enters the brain within the perivascular spaces of arteries, while interstitial fluid drains along perivascular venous sector. Moreover, it has been showed that vascular basement membranes have a complex multi-layered architecture that originates with epithelial, endothelial, smooth muscle cells and glial cells, and that the virtual space between these layers might be in fact an essential component of these perivascular spaces. Starting from a patient that presented with active pulmonary tuberculosis and with consecutive purulent-hemorrhagic meningitis and encephalitis, we have characterized here the compartments in which immune cells can be found in the brain tissue. Besides the classical histopathological description, what was of interest here, was that we identified for the first time mononucleated inflammatory cells that seemed to be present in pockets of the vascular basement membranes, small spaces devoid of red blood cells. Although this is mere a morphological observation, future high-resolution studies should clarify it this is a possible route for the immune cells entering the brain.