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Peripheral blood lymphocytes (PBL) from 24 allogeneic bone marrow transplant (BMT) recipients were studied serially using flow cytometry and two-color analysis. Dual labelling with two monoclonal antibodies (moAbs), CD8/S6F1 (CD11a) and CD8/CD57 was used to analyze the surface phenotypes of PBL after allogeneic BMT. In patients with acute and chronic GVHD, CD8+S6F1+ cells were markedly increased from the onset of GVHD and recovered to normal range 6 years after transplantation. By contrast, CD8+S6F1- cells fell below normal range and remained markedly decreased for 2-3 years after transplantation in patients with acute and chronic GVHD. A slight but significant increase of CD8+CD57- cells was observed with clinical signs of acute GVHD. On the other hand, CD8+CD57+ cells were increased after the onset of acute and chronic GVHD and recovered to normal range 6 years after transplantation. These results suggest that these subsets of CD8+ cells may play important roles in the pathophysiology of GVHD.

We used a thin-sectioning technique for the electron microscopic detection of viral particles within the cells of urinary sediments in three recipients who developed hemorrhagic cystitis after allogeneic bone marrow transplantation. Results of viral cultures of urine and electron microscopic (EM) observations on urinary sediments were consistent in only one recipient. In this recipient, EM observations revealed many viral particles within the cells of urinary sediments with diameter of about 80 nm corresponding to adenovirus, of which type 11 was produced in viral cultures. In one of the other two recipients many viral particles with a mean diameter of 41.6 nm corresponding to papovavirus were observed, but viral cultures using conventional cells were negative. Re-cultures using HEK cells produced polyomavirus BK. EM observation was a clue to the correct diagnosis. In the remaining recipient, no viral particles were observed within the cells of urinary sediments, suggesting the hemorrhagic cystitis to be of non-viral origin, despite a positive result of viral culture. These results suggest that a thin-sectioning technique on the cells of urinary sediments is important for the differential diagnosis between a viral-induced and non-viral hemorrhagic cystitis.

A patient with acute myeloid leukemia (M4) in the first complete remission received a bone marrow transplantation (BMT) from an HLA-compatible sibling. Sustained engraftment was achieved, but she developed colicky pain at the back and lower quadrant of both sides on days 19-21 post-BMT, followed by hemorrhagic cystitis 13 days later. Ultrasonogram, intravenous pyelogram and computed tomogram of the abdomen showed hydronephrosis and ureteric obstruction of both sides. There was no stone in the urinary tract or abnormality of the bladder. The cortex of the right kidney was rather hypertrophic in spite of the persistent presence of hydronephrosis. Viral culture of urine and electron microscopic examination of urine sediments revealed the presence of adenovirus type II. Infection of the urinary tract with adenovirus type II may have been the underlying cause of the hemorrhagic cystitis and possibly also of the otherwise unexplained ureteric obstruction.

One hundred and four patients with acute leukemia treated by allogeneic bone marrow transplantation in Japan were analysed for the incidence of interstitial pneumonitis (IP). Thirty-six (35%) of 104 marrow graft recipients developed IP. Cytomegalovirus (CMV) was the most frequent organism (61%). Using multivariate analysis, remission at transplant (P = 0.0001) and use of cyclosporin A to prevent graft-versus-host disease (P = 0.0363) were found to be significant factors associated with a decreased incidence of IP. For preventing IP, anti-CMV hyperimmune globulin was effective, while interferon and acyclovir were not.