Chromosome studies were conducted on 15 patients with adult T‐cell leukemia. Cells with chromosomal abnormality were seen in 14 of the 15 patients. The modal chromosome number was near diploid range in all the patients. The most common abnormality was 14q+ marker chromosome and partial deletion of the long arm of chromosome 6, i.e., 6q‐, which were seen in eight and seven cases, respectively. Donor chromosomes involved in the 14q+ marker chromosome varies, i.e., Yq, #5p, #5q, #9q, #10q or #12q, except for two patients whose donor chromosome origins were unable to determine. The break point in 14q+ marker chromosome was band at q32. The 6q‐ chromosome was due to a deletion in one patient and interstitial deletion in six patients. A 14q‐ chromosome having break point at q24 was found in one patient and duplication of Yq chromosome in two patients. In addition, four patients showed a 5q‐ chromosome or a 9q‐ chromosome which was due to a translocation or deletion. The significance of these chromosome abnormalities was discussed.
SummaryThe vitamin B12 levels of cerebrospinal fluid were assayed microbiologically (Lactobacillus leichmannii method) using samples from 44 patients with various neurological disorders, 4 patients with megalo blastic anemia and 34 controls. Twenty-seven controls that did not receive vitamin B12 showed a mean cerebrospinal fluid vitamin B12 level of 21.5pg/ml (range: 0-60). No decrease in cerebrospinal fluid vitamin B12 level was seen in patients with subacute myelo-optico-neuropathy (SMON). High levels of cerebrospinal fluid vitamin B12 were observed only in the patients receiving long term administration of the vitamin. Intrathecal administration of vitamin B12 caused only a slight increase in serum vitamin B12 level after four hours. The existence of a blood brain barrier for vitamin B12 was suggested.
We describe a patient with allergic granulomatous angitis who developed autoimmune hemolytic anemia (AIHA). A 44-year-old male had been suffering from bronchial asthma. On admission, laboratory tests revealed the presence of severe eosinophilia (21,500/microliters), elevation of total immunoglobulin E (IgE), high lactic dehydrogenase (LDH) and low haptoglobin levels, in addition to moderate reticulocytosis. During admission, the patient showed almost simultaneous occurrence of vasculitis in the extremities, severe hemolysis and exacerbation of asthma in relation to the progression of eosinophilia. Both IgM and IgG autoantibodies were considered to be responsible for hemolysis. Interestingly, serum levels of interleukin-4 (IL-4) and IL-5 were increased in association with eosinophilia and increased IgE production. These findings suggest that the AIHA in this patient is mediated or enhanced at least partly by high IL-4 and IL-5 production. Although AIHA in this syndrome is very rare, it should be considered as a clinical manifestation.
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