Biomedical subjects
Publications and source records attributed to J Otten.
A 14-month-old boy with neurofibromatosis and skin xanthomas associated with normal lipemia is described. Acute lymphocytic leukemia complication and its connection with the cutaneous disease are discussed.
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Two hundred and seventeen patients, 1-50 yr old, with acute lymphoblastic leukemia in complete remission were randomized to receive a 1-yr consolidation chemotherapy of either type P, comprising 7 different drugs, or type M, consisting of methotrexate interspersed with prednisone and vincristine. Thereafter, they were randomized a second time to receive a 4-yr maintenance of either chemotherapy or immunotherapy, comprised of allogeneic blasts and bacillus Calmette-Guérin (BCG). Consolidation P caused more toxicity than consolidation M. However, comparison between the consolidation therapies P and M showed no significant difference, neither for disease-free interval nor for duration of survival. Chemotherapy showed more lethal toxicity in adults than in children. Comparison between chemotherapy (C) and immunotherapy (I) as maintenance treatment showed a significant (p = 0.016) superiority of C for disease-free interval (DFI). The difference was even more pronounced (p = 0.009) in the group with less than 8 g/dl of hemoglobin (Hb) at diagnosis before therapy. On the other hand, for patients with more than 8 g/dl Hb at diagnosis, presumably those with T-ALL, no difference in DFI was seen. No difference has been seen so far between maintenance therapies I and C concerning the duration of survival. The patients who were receiving maintenance I when they relapsed and who were consequently retreated by chemotherapy, survived longer from relapse than those patients retreated for relapse while receiving maintenance C.
In a sporadic case of primary maxillar Burkitt's lymphoma and secondary spinal epidural dissemination, the massive malignancy in the CSF was investigated by light and electron microscopy. At both levels the CSF tumor cells were strikingly similar, with the undifferentiated lymphoblasts that characterize Burkitt's lymphoma in tissue. However, the starry-sky appearance in the CSF was produced more often by degenerating malignant cells than by histiocytes as classically described in tissue with Burkitt's lymphoma.
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In a patient with systemic and nervous system IBS, the CSF cells were investigated by light and electron microscopy. An IBS of the B-cell type was identified in the CSF which proved, at both morphological levels, to be identical to that recorded in IBS in lymphoid tissue with regard to the malignant cell types and the absence of surface specialization. In contrast, unusual macrophages were observed in the CSF instead of the reticular elements associated with IBS in lymph nodes which present desmosomes. They demonstrated both phagocytosis and emperipolesis and also displayed autodesmosomes. The CSF phagocytes are discussed in relationship with the phagocytes described in the brain with malignant lymphoma.
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Peptichemio (PTC) was utilized in various advanced and disseminated tumors in children. With the schedule that was used, toxicity was mild. Immediate side effects included anaphylactoid reactions which required close supervision of the patient during infusion of the drug. PTC proved efficacious in advanced neuroblastoma. In patients with bone metastases, PTC has a prompt analgesic effect which seems to occur independently of any antitumor action.
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Urinary cyclic adenosine 3'5' monophosphate (AMP) excretion has been determined by radioimmunoassay in children with rickets and in control children. Cyclic AMP was greatly increased in children with rickets. The excretion of cyclic AMP correlated significantly with parathyroid hormone levels (PTH) and alkaline phosphatase, but not with age, calcaemia and serum inorganic phosphate. Calcium infusion led to a decrease in the excretion of cyclic AMP. The data are consistent with following hypothesis. During vitamin D deficiency, high PTH levels can increase the renal excretion of cyclic AMP. The effects of PTH on bone resorption fail to maintain the levels of serum calcium due to the lack of vitamin D. The mechanism by which the secondary hyperparathyroidism develops during vitamin D deficiency remains to be investigated.
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