PubMed Health⌕ Search

Biomedical subjects

L Kolodie

Publications and source records attributed to L Kolodie.

28 records · Page 2Linked to original sources
PubMedDate not supplied

[Thrombocytosis and reduced levels of factor VIII in rheumatoid purpura in children].

Thirty three patients with Henoch-Schoenlein purpura were studied at various developmental stages of this disease: specially platelet counts and factors XIII and VIII. During the development phases: 40,6% of the patients have a slight but regressive thrombocytosis (greater than 400 G/l); and 75% a reduced factor XIII, well correlated with the severity of the clinical status (level as low as 60% can be considered as a "gravity threshold"), and corrected during the improvement of the disease. This reduced factor XIII is probably linked to the local inflammation in the vessels. Factor VIII studies (specially VIII A: Ag) were normal.

Adolescent↗
PubMedDate not supplied

[Must we teach, today, the MCHC (Mean Corpuscular Haemoglobin Concentration)? (author's transl)].

Automatic cell counters introduce a new interpretation of the MCHC. The automatic MCHC does not fall in cases of thalassemia or of iron deficiency, except in the severest; so it serves now little practical purpose. The manual MCHC continues to be a useful index of hypochromia, but does not reflect the true haemoglobin concentration in red cells, and it remains less and less in use.

Anemia, Hypochromic↗
PubMedDate not supplied

[Study of the fibrin degradation products in the synovial fluid of rheumatological diseases (author's transl)].

FDP were studied in the synovial fluid of 23 patients with various rheumatological diseases. The levels, measured by the passive hemagglutination inhibition technique (Merskey technique), showed variable values, but were always found to be present. On half the cases a number of these molecules could be eliminated by a high dose of thrombin. Using three immune sera (anti-fibrinogen, anti-D, anti-E), immunoelectrophoresis revealed in half the cases one central nonmigrating arc and another with cathodic migration. This differs from results using FDP obtained by the digestion of fibrinogen by plasmin, but is, however, analagous with those obtained in vitro by the action of proteases of leukocyte origin. These results suggest that the intense fibrinogen catabolism within the pathological joints results from the action of proteolytic enzymes other than plasmin.

Fibrin Fibrinogen Degradation Products↗