Mesna and forced diuresis are equally effective in abrogating the urothelial toxicity of preparative regimens for BMT. Since HC after BMT is virtually always associated with persistent BK viruria, strategies aimed at the prevention or elimination of viruria in BK seropositive recipients are warranted.

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Serums of patients with hereditary angioneurotic edema lack inhibitory activity against the esterase derived from the first component of complement. In one group of patients this lack appears to result from failure to synthesize the esterase inhibitor of the first component of complement, whereas in another group of patients an abnormal, nonfunctional protein is synthesized.

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EBV DNA has been detected by Southern blot hybridization in 20-25% of Hodgkin's disease tumor specimens and localized to the Reed-Sternberg cells by in situ hybridization. In the present investigation we used a 3H-labelled EBER I anti-sense RNA for in situ hybridization of archival formalin-fixed paraffin-embedded Hodgkin's disease specimens previously shown by Southern Blot hybridization to be EBV-positive. In 6 of 8 specimens neoplastic cells showed an intense signal in virtually all of the tumor cells. The background lymphocytes, eosinophils, plasma cells and histiocytes did not demonstrate significant hybridization. In each case hybridization tended to spare the nucleoli. Hybridization was detected in specimens with histologies of mixed cellularity and nodular sclerosis. The intensity of signal relative to background is better than that in previous studies utilizing 35S-labelled large internal repeat probes for EBV in Reed-Sternberg cells. The exposure time is one week in contrast to the 4-5 weeks reported by others for detection of EBV in Hodgkin's disease. Both increased relative intensity and shorter exposure requirements may be attributed to the very high number of EBER transcripts in the target cells. The demonstration that EBER I is expressed is consistent with a role for EBV in growth regulation of Reed-Sternberg cells and suggests that the virus is not merely a silent passenger in Hodgkin's disease.

Fifty-five recipients of bone marrow transplants were monitored prospectively for urinary excretion of BK (BKV) and JC (JCV) viruses and for infections with other viruses. For both BKV and JCV, viruria occurred exclusively in patients who were seropositive at transplantation, a finding indicating that shedding of virus was very likely the result of reactivation. BKV reactivation, which occurred in 26 (55%) of 47 BKV-seropositive patients, was far more common than JCV reactivation, which was detected in only two (7%) of 30 JCV-seropositive patients (P less than .0001). In most patients, BK viruria began two to eight weeks after transplantation and resolved spontaneously after a two- to three-week period. Posttransplantation, there was a temporal pattern in the onsets of infection with the different viruses; herpes simplex virus infections occurred first (mean, 7 d), followed by BKV infections (mean, 33 d) and then cytomegalovirus infections (mean, 51 d). BK viruria was associated with hemorrhagic cystitis.

Clinicians at the bedside can use readily available clinical and laboratory information to decide which patients are likely to have C. difficile disease and when it is appropriate and useful to order specific diagnostic tests for C. difficile toxin. Such data are also useful in determining the number of stool samples that reasonably excludes the diagnosis of C. difficile colitis.