Following extensive bowel resection, a young woman experienced severe malnutrition; subsequent administration of parenteral nutrition precipitated the copper deficiency syndrome. This consisted of hypocupremia, subnormal ceruloplasmin levels, anemia, and severe neutropenia. The bone marrow was megaloblastic, vacuolated, and sideroblastic; granulocytic maturation was not observed beyond the myelocyte stage. Copper sulfate therapy was followed by a marked reticulocytosis, increase in hematocrit, and recovery of neutrophils. Additional studies indicated that both serum and urinary erythropoietin values were low; serum activity increased after copper supplementation. Abnormal granulopoiesis was demonstrated using the in vitro granulocyte colony assay. The patient's granulcoytic stem cells were normal on two occasions; however, mixing studies showed that culture of the patient's copper-deficient marrow with her copper-deficient serum yielded significantly reduced numbers of granulocyte colonies. Thus, copper appears to be a necessary element for normal hematopoiesis; lack of this trace element may result in ineffective erythropoiesis and granulopoiesis.
Cisplatin was given intravenously to 35 evaluable patients with unresectable malignant mesothelioma on Southwest Oncology Group (SWOG) Study 8418. Five patients (14.3%) achieved partial response with median response duration of six months (range 2-12 months); eleven patients (31.4%) had stable disease of median duration of 5.5. months (range 2-21 months). Median survival for all patients was 7.5 months, 9 months for responders. Toxicity was as expected except that 12 patients (34.2%) discontinued cisplatin because of side effects. Cisplatin has moderate activity in mesothelioma and further studies with platinum analogues should be pursued.
The authors report a case of a collision tumor composed of a primary gastric rhabdomyosarcoma intermingled with an adjacent infiltrating gastric adenocarcinoma. Only eight cases of gastric rhabdomyosarcoma have been reported previously and little information is recorded about the behavior of this tumor. Gastric rhabdomyosarcoma has several distinctive clinical features. It is a highly aggressive tumor (median survival, 2.5 months) occurring in both children and adults and frequently presents as metastatic disease to lung or cervical lymph node. The initial diagnosis is often difficult to establish, especially on biopsy material. In several instances, the correct diagnosis was established only at autopsy. The authors' patient was correctly diagnosed during life and received considerable benefit from cyclophosphamide, doxorubicin, and vincristine (CAV) therapy and survived for 26 months after diagnosis. Two of the previously reported eight cases of primary gastric rhabdomyosarcoma and this case have adjacent admixed glandular gastric adenocarcinomas. Since three of the nine known cases of primary gastric rhabdomyosarcoma have an adjacent admixed gastric adenocarcinoma, there appears to be a greater than chance association between these two tumors.
The authors studied an 18-year-old woman with stage IIIB nodular sclerosis Hodgkin's disease whose bone marrow contained abnormal storage cells that resembled Gaucher cells by light microscopic examination ("pseudo-Gaucher" cells). Electron microscopic examination revealed that these cells differed from true Gaucher cells and resembled storage cells previously described in chronic myelogenous leukemia. The patient's peripheral blood leukocyte beta-glucosidase and serum acid phosphatase levels were elevated, ruling out the diagnosis of inherited Gaucher's disease. After treatment with six monthly cycles of systemic chemotherapy (nitrogen mustard, vincristine, procarbazine, bleomycin, doxorubicin, and prednisone), all signs of Hodgkin's disease and pseudo-Gaucher cells disappeared. Repeat leukocyte beta-glucosidase and serum acid phosphatase levels were unchanged. The present case is unique with its documentation of classical enzyme patterns for beta-glucosidase and acid phosphatase and electron microscopic features. The authors postulate that pseudo-Gaucher cells result from excessive cell breakdown with an overload of available beta-glucosidase.
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