Carpal tunnel syndrome, peripheral arthropathy, erosive spondiloarthropathy and lytic bone lesions have all been associated with dialysis amyloidosis. Recent studies indicate that β2-microglobulin is the major constituent protein in this new form of amyloidosis. Dialysis amyloidosis was reported to have a local rather than a systemic involvement, although its full extent is yet to be determined. We investigated 3 patients on maintenance hemodialysis with bilateral caφal tunnel syndrome and amyloid arthropathy and found amyloid depositions in several organs. These findings suggest that, in contrast to what had been thought previously, dialysis amyloidosis could have systemic as well as visceral distribution. The amyloid deposits found were resistant against potassium permanganate treatment and reacted with anti-human β2-microglobulin antibody.
Summary.A female patient with delayed haemolytic transfusion reaction due to anti-M antibody is described. Diagnosis was based on laboratory evidence of haemolysis and on characteristic serological findings. Anti-M was detected in the recipient's serum 7 d after the last transfusion episode. This alloantibody had not been present in the pretransfusion serum. In addition, the direct antiglobulin test was positive on post-transfusion testing and the implicated antibody was eluted from post-transfused red cells.Delayed haemolytic transfusion reactions have long been recognized as a potencial hazard of transfusion therapy, but such cases due to anti-M are extremely rare.
Diffuse alveolar damage (DAD) is the underlying pathological finding in most cases of acute respiratory distress syndrome (ARDS). The objective of this study was to compare clinical criteria for ARDS secondary to community acquired pneumonia with autopsy findings of DAD and to determine the discrepancy rate between the two. We compared prospectively obtained clinical diagnosis of ARDS secondary to community acquired pneumonia with autopsy findings of DAD and pneumonia. Forty nine patients dead with a clinical diagnosis of ARDS secondary to pneumonia who underwent autopsy between 1986 and 2004 in our ICU were included with systematic histopathological analysis of all lung lobes. The discrepancy rate between the premortem clinical diagnosis of ARDS secondary to pneumonia and DAD at autopsy was determined. Seven patients were found to have neither infection nor DAD at autopsy. Six patients showed pathologic signs of DAD without evidence of infection. Out of 38 patients meeting clinical criteria for ARDS secondary to pneumonia and proven pneumonia at autopsy, 25 met criteria for DAD at autopsy. Therefore, 18 out of 49 patients who were clinically diagnosed with ARDS did not actually show pathological signs of DAD, resulting in a discrepancy rate of 37%. Despite an acceptable correspondence between clinical criteria for ARDS secondary to pneumonia and autopsy findings of DAD a significant number of patients had neither signs of DAD nor infection.
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