The proinflammatory cytokines IL-1beta, IL-8, and TNF-alpha play a major role in the process of bone resorption during aseptic loosening of large joint prostheses. These cytokines secreted locally during bone resorption in aseptic loosening may enter peripheral circulation. Increased concentration of IL-1gamma, IL-8, and TNF-alpha in peripheral circulation may indicate aseptic loosening. We determined whether bone resorption could be verified by cytokine presence in plasma. We recruited 50 patients with aseptic prosthesis loosening, 50 with stable prostheses, 50 with osteoarthritis, and 50 healthy individuals. Cytokine levels were determined in plasma by ELISA tests. Patients with prosthesis loosening had higher plasma levels (IL-10, 3.7 +/- 5.5 pg/mL; IL-8, 14.7 +/- 9 pg/mL; TNF-alpha, 32.7 +/-+/- 32.4 pg/mL) than patients with stable prostheses (IL-1beta, 1.5 +/- 2 pg/mL; IL-8, 8.1 +/- 4.7 pg/mL; TNF-alpha, 22.9 +/- 18.7 pg/mL), patients with osteoarthritis (IL-1beta, 0.7 +/- 1.1 pg/mL; IL-8, 5.8 +/- 3.8 pg/mL; TNF-alpha, 9.8 +/- 7.7 pg/mL) and healthy individuals (IL-1beta, 0.7 +/- 1.1 pg/mL; IL-8, 4.2 +/- 1.3 pg/mL; TNF-alpha, 3.9 +/- 3.9 pg/mL). Our data suggest elevated plasma levels of proinflammatory cytokines may be useful as markers of bone resorption in the laboratory diagnosis of prosthesis loosening.

The possibility of controlling the harmful intraarticular influence of elevated interleukin (IL)-1β synovial fluid concentration after anterior cruciate ligament (ACL) surgery could be useful. We investigated the correlation between serum and synovial fluid IL-1β levels following ACL reconstruction. We measured IL-1β concentration periodically in three synovial fluid and four serum samples in each of 20 patients receiving either autologous conditioned serum (ACS) containing endogenous anti-inflammatory cytokines including IL-1Ra and several growth factors (group A) or placebo (group B). A decrease in IL-1β synovial fluid concentration appeared to be more pronounced in absolute terms in group A. In eight patients serum IL-1β was detected on the 6th postoperative day. In four of them whose synovial fluid levels were over 10 pg/ml on the 6th postoperative day, serum IL-1β was detected on the 10th postoperative day. The results were different in group B. Correlation between serum and synovial fluid IL-1β appearance persists in patients after ACL surgery and ACS application. This study is an example of ACS influence on the ACL healing process controlling the IL-1β levels on the basis of the serum IL-1β detection.

Dear Sir,The Rh blood group system is determined by the highly homologous RHD and RHCE genes located on the first chromosome, which encode for the RhD and RhCE polypeptides. D antigen is of special clinical relevance in the fields of transfusion medicine and obstetrics. Owing to its high immunogenicity, D antigen can induce the production of alloantibodies and thus cause posttransfusion haemolytic reaction and haemolytic disease of the newborn (Wagner et al., 2000).About 0·2-1% of the European population are carriers of structurally altered RHD alleles encoding for various types of weak D proteins. At the molecular level, point mutations resulting in amino acid substitutions in the intracellular or transmembranous segments of RhD protein are causing weak D phenotypes. More than 170 different RHD alleles closely related to the expression of the respective D phenotype, including more than 70 weak D types, have been discovered to date (Flegel, 2007). Some weak D types (types 1, 2 and 3) are not associated with the development of alloantibodies; however, alloimmunisation in weak D types 4·2, 11 and 15 carriers have been reported (Flegel, 2006). Owing to the extremely small phenotypic variation, particular weak D types are very difficult to differentiate by serology and can only be identified by molecular methods, thus enabling definitive decision on the mode of transfusion treatment and the need of anti-D prophylaxis in pregnant women. The individuals who are carriers of weak D types 1, 2 and 3 can receive transfusion of D+ red blood cell (RBC) units, although such pregnant women do not require anti-D prophylaxis. Thus, the unnecessary utilisation of D− RBC units and RhIg is avoided (Flegel and Wagner, 2002).Particular segments of the RHD gene sequence are multiplied by RHD genotyping using primers specific for the known mutations characterising particular weak D types by use of the polymerase chain reaction with sequence-specific priming (PCR-SSP). This procedure is employed to determine polymorphism of the weak D types.

Neonatal alloimmune neutropenia-incidence, serologic diagnosis, antineutrophil antibodies, anti-HNA, anti-HLA class I, Croatia.

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Alloimmune neonatal neutropenia (ANN) is a rare but potentially life-threatening disorder of neonates. Demonstration of alloantibodies against granulocyte-specific antigens shared by neonatal and paternal granulocytes in the maternal serum is essential in the diagnosis of ANN. In contrast to granulocyte-specific alloantibodies, the significance of human leucocyte antigen (HLA) class I antibodies for ANN is still a matter of debate. We report on a case of severe isolated and prolonged neutropenia due to anti-HLA B49 alloimmunization only. Immediately after birth, severe, isolated neutropenia was observed and lasted for up to 2 months. Results of serologic testing showed only anti-HLA B49 antibodies in the maternal and neonate's sera. HLA typing showed HLA class I (B49) incompatibility between the mother and the child. Granulocyte-specific antibodies were not detected. Adsorption of the maternal serum with HLA B49-bearing platelets removed serum reactivity with paternal neutrophils. Our results support the idea that certain HLA class I antibodies can induce ANN.

Alloimmunization to granulocyte-specific antigens can occur during pregnancy. Maternal antibodies of IgG class can cross the placenta to result in alloimmune neonatal neutropenia. Antibodies to human neutrophil antigens anti-HNA-1a, HNA-1b, and HNA-2a have been most commonly reported to cause alloimmune neonatal neutropenia. Isoantibodies to Fc gamma RIIIb (CD16) if mother is a HNA-null phenotype are rarely involved in neonatal neutropenia. We report on a case of severe neutropenia (440 neutrophils/μL) due to anti-Fc gamma RIIIb (CD16) isoimmunization. On day 14 severe omphalitis developed, which was treated for 7 days by an antibiotic (ceftriaxone in a dose of 80 mg/kg/d) according to umbilical swab finding. Omphalitis persisted for 10 days in spite of antibiotic therapy and only resolved upon the introduction of rhG-CSF therapy. Therapy with rh-GCSF proved efficient and led to neutrophil count increase to 1970/μL and cure of omphalitis. However, therapeutic effect on granulocyte count was of transient nature, as granulocyte count fell to 760 n/μL on day 4 of therapy discontinuation. Neutropenia persisted for 2 months. The newborn was discharged from the hospital on day 26 with normal clinical status with clinical and laboratory control examinations at 2-week intervals. No additional infections were observed during the course of neutropenia.