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Neuropsychological performance in 20 chronic schizophrenic patients was contrasted to 25 Parkinson's disease, 12 Huntington's disease patients and 26 normal controls on measures shown to be sensitive to subcortical dysfunction. Some overlap was observed in the performance of the schizophrenic and basal ganglia groups on tasks of executive and mnestic function, but the general pattern indicated significant differences in performance. Notably, in contrast to the two basal ganglia groups, there was no evidence of slowed thinking, or impaired motor function in schizophrenia, which are considered hallmarks of subcortical grey matter disease. An association was observed between poor performance on the tests of executive function and the severity of negative symptoms. Our findings suggest that schizophrenia is not associated with primary subcortical impairment, but is more likely to reflect frontotemporal dysfunction. We consider that the similarities between this disorder and subcortical degenerative syndromes may be due to a difficulty in generating action in schizophrenia, perhaps arising from dorsolateral prefrontal disconnection.

The association of polyomaviruria and microscopic haematuria was studied by the use of electron microscopy (EM) and the polymerase chain reaction (PCR) in bone marrow transplant (BMT) recipients. The incidence of BK virus (BKV) and JC virus (JCV) excretion was further elucidated by means of restriction enzyme analysis of the PCR products. Polyomaviruses were detected in 43 (51.2%) of the 84 samples, 13 (30.2%) of which had a virus concentration detectable by EM. By typing with BamHI cleavage, 29 (67.4%) of the 43 positive patients were found to be excreting only BKV and the remaining 14% (32.6%) were excreting both BKV and JCV. Microscopic haematuria was present in 17 (20.2%) of 84 urine samples collected from different patients within 4 months post-transplant. The incidence of microscopic haematuria was significantly higher, 34.9% (P0.01), in patients with polyomaviruria than in those without (4.9%) but no difference was observed between the BKV-excreting and BKV/JCV-co-excreting patients. Microscopic haematuria was not present, however, in 53.8 and 65.2% of polyomavirus-excreting patients when virus was detected by EM and PCR respectively. While most episodes of microscopic haematuria observed were self-limiting and asymptomatic, three patients excreting polyomavirus had symptoms of cystitis and one of them had renal impairment that was otherwise unexplained. We thus conclude that polyomaviruses probably contribute to damage of urinary tract tissue in some BMT recipients.

Summary The authors report the clinical, pathological and immunological features of a case of T-lymphoblastic lymphoma presenting with protein-losing enteropathy. There was extensive multifocal involvement of the duodenum, jejunum and ileum. The mediastinum was not enlarged; the peripheral blood picture and bilateral bone marrow trephine biopsies were unremarkable. The tumor cells were positive for terminal deoxynucleotide transferase, CD3, CD2, CD7 and CD10; they were negative for CD1, CD5, CD4, CD8 and HLA-DR. The immunophenotype was that of an immature thymic T-cell. Monocytic and B-cell markers were negative. Despite initial dose reduction in chemotherapy, the patient still developed massive intestinal hemorrhage and succumbed 2 wks after treatment. Postmortem examination confirmed absence of thymic involvement. The overall picture strongly suggests a primary intestinal origin of this T-lymphoblastic lymphoma which contradicts the conventional wisdom that T-lymphoblastic lymphoma arises in the thymus from primitive cortical lymphocytes before rapidly disseminating.

One hundred Chinese patients who received induction cytotoxic therapy for malignant lymphoma were prospectively studied to determine the incidence, morbidity, mortality, and predisposing factors for reactivation of hepatitis B virus replication during cytotoxic therapy. In 18 (67%) hepatitis B surface antigen-positive and 10 (14%) hepatitis B surface antigen-negative patients, hepatitis developed during cytotoxic therapy (P less than 0.0001). Hepatitis could be attributed to exacerbation or reactivation of chronic hepatitis B in 13 (72%) hepatitis B surface antigen-positive patients but in only 2 (20%) hepatitis B surface antigen-negative patients (P less than 0.0001). Sudden increase or reactivation of hepatitis B virus replication gave rise to icteric hepatitis, nonfatal hepatic failure, and death in 22.3%, 3.7%, and 3.7% of patients who were positive for hepatitis B surface antigen; in 2%, 2%, and 0% of those positive for hepatitis B antibodies; and in none of those who were seronegative. Among the hepatitis B surface antigen-positive patients, male sex was the only factor that was associated with an increased risk of reactivation of hepatitis B virus replication. We recommend that hepatitis B surface antigen-positive patients with malignancies receiving cytotoxic therapy be closely monitored.