Key Points Antibodies causing FNAIT have decreased Fc fucosylation, unlike in refractory thrombocytopenia. Decreased Fc fucose increases affinity to FcγRIIIa/b, enhances platelet phagocytosis, and correlates with increased disease severity.

The study's objective was to identify HPA 1a-negative women and to offer them an intervention program aimed to reduce morbidity and mortality of neonatal alloimmune thrombocytopenia (NAIT). HPA 1 typing was performed in 100 448 pregnant women. The HPA 1a-negative women were screened for anti-HPA 1a. In immunized women, delivery was performed by Cesarean section 2 to 4 weeks prior to term, with platelets from HPA 1a-negative donors reserved for immediate transfusion if petechiae were present and/or if platelet count was less than 35 ؋ 10 9 /L. Of the women screened, 2.1% were HPA 1a negative, and anti-HPA 1a was detected in 10.6% of these. One hundred seventy pregnancies were managed according to the intervention program, resulting in 161 HPA 1a-positive children. Of these, 55 had severe thrombocytopenia (< 50 ؋ 10 9 /L), including 2 with intracranial hemorrhage (ICH). One woman with a twin pregnancy missed the follow-up and had one stillborn and one severely thrombocytope-

Experimental amyloidosis was induced in mice by intraperitoneal injections of endotoxin (lipopolysaccharide (LPS)). In addition to LPS, a group of mice received high-density lipoprotein (HDL)-SAA complexes isolated from human acute-phase serum, whereas a group of control mice received saline in addition to LPS. Isolated amyloid fibrils from the mice given HDL-SAA contained human AA protein, as shown by immunodiffusion, immunoblot, and enzyme-linked immunosorbent assay techniques, in addition to mouse AA. In contrast, amyloid from the control mice contained exclusively AA of mouse origin. Thus, the experiments provided solid evidence that SAA is the precursor for amyloid fibril protein AA.