Biomedical subjects
P Resnitzky
Publications and source records attributed to P Resnitzky.
[Severe side-effects of captopril].
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High incidence of acute myeloid leukemia in SJL/J mice after X-irradiation and corticosteroids.
SJL/J mice which developed a high incidence of spontaneous reticulum cell neoplasms, developed a low rate incidence (20-25%) of myeloid leukemia (ML) after X-irradiation. The possible effect of adrenal steroid imbalance to radiation-induced ML in SJL/J mice was tested. Intact and thymectomized animals were exposed to a single dose of 300 r whole body irradiation and treated with either hydrocortisone acetate, prednisone, metyrapone and adrenocorticotropin as coleukemogenic agents. Hydrocortisone and prednisone exerted a marked coleukemogenic effect, increasing the ML incidence to a similar rate of about 50-70%, at a mean latent period of 300 days. Prominent leukemic infiltration were observed in the bone marrow, spleen, lymph nodes and liver of the leukemic animals. Results of cytological and histological studies, including cytochemistry and ultrastructure, were all consistent with the diagnosis of acute myeloid leukemia (AML). Since AML is the type of human secondary leukemia which appears increasingly in patients treated with alkylating drugs and/or irradiation and corticosteroids for Hodgkin's disease or other neoplastic diseases, the experimental model of AML induced in SJL/J mice could be used for elucidation of mechanisms of leukemogenesis in secondary leukemia.
In vitro functions of stromal cells from human and mouse bone marrow.
Human fibroblastoid cell strains obtained from primary bone marrow cultures and continuous stromal cell lines recently derived from mouse bone marrow were studied. The incidence of fibroblastoid precursors (CFU-F) varied considerably in human bone marrow samples, and no differences could be detected between marrows from a group of myelodysplastic patients (age range 70-82 years) and groups of age-matched controls or younger individuals. A lack of direct correlation between initial clonogenicity and ultimate capacity of fibroblastoid cells to grow in continuous culture was observed in both the normal and the myelodysplastic groups. Despite the apparently normal clonogenicity of CFU-F in patients with myelodysplastic syndromes, some of these marrows failed to grow when subcultured. Normal fibroblastoid cells at 10(4) per culture exhibited myelopoietic activities when cocultured with fresh bone marrow cells. At higher concentrations, these cells inhibited myeloid colony formation. Fibroblastoid cells from only one out of four myelodysplastic patients examined exhibited comparable inhibitory activity. The specificity of the inhibitor(s) was demonstrated by the lack of effect of fibroblastoid cells from normal human bone marrow on the clonogenicity of mouse erythroleukemia cells. Moreover, human foreskin fibroblasts were devoid of such inhibitory activity. These functions of cultured stromal cells may correlate with some of their activities in the bone marrow microenvironment.
Platelet aggregation defect in megakaryoblastic leukemia.
Platelet aggregation induced in vitro with ADP, adrenalin and ristocetin was tested in 7 patients with megakaryoblastic leukemia (MKL). All patients had normal or high platelet counts and presented with hemorrhagic diathesis including purpura ecchymosis and epistaxis. Platelet morphology was grossly abnormal and electron microscopy revealed few, or absence of, alpha-granules. Platelet aggregation was reduced in all the cases with at least one aggregating agent. Our studies confirm that MKL is often accompanied by a thrombocytopathy which should be taken into account in the management of these patients.
Candidemia and sternal Candida albicans osteomyelitis in a patient with chronic lymphatic leukemia.
Sternal osteomyelitis caused by Candida albicans without previous surgery or trauma occurred in a patient with chronic lymphatic leukemia and recurrent skin cancer. The osteomyelitic process healed without antifungal treatment. Three weeks later, following a radical neck dissection, candidemia, without recurrence of the osteomyelitis, was diagnosed and treated successfully with intravenous amphotericin B and 5-fluorocytosin. The presentation of Candida osteomyelitis as a manifestation of disseminated candidiasis in immunocompromised hosts is discussed and the relevant literature is briefly reviewed.
Histiocytic hemophagocytosis in Q fever.
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IgM lambda globular cytoplasmic inclusions in chronic lymphocytic leukaemia resembling immunocytoma.
In a 64-year-old female with chronic lymphocytic leukaemia, nearly 50% of the lymphocytes presented one or several globular intracytoplasmic inclusions resembling Russell bodies which were characterized by immunofluorescence as IgM lambda. On electron microscopy, the inclusions looked like cisternae of the rough endoplasmic reticulum. Surface membrane Ig was not detected and the serum IgM was low. The histology of a lymph node showed a lymphocytic proliferation with evidence of Ig synthesis, compatible with immunocytoma. The aggressive course of the disease necessitated polychemotherapy. This case represents an unusual ill-defined lymphoproliferative disorder, lying between the B-CLL and a non-secretory macroglobulinaemia.
Enhancement of hemopoietic stem cell proliferation by prostaglandin inhibitory drugs.
The in vivo effect of several prostaglandin inhibitory drugs on the hemopoietic stem cell was studied in SJL/J mice. Repeated intramuscular administration of Indomethacin increased the total number of bone marrow (BM) and spleen pluripotent hemopoietic stem cells (CFUS). The number of spleen colonies in lethally-irradiated normal BM recipients, which had been treated with Indomethacin, Aspirin or Flufenamic acid (all prostaglandin inhibitory drugs), was significantly greater than controls' spleen colonies. After exposure of SJL/J mice to different amounts of irradiation, more endogenous spleen colonies and a greater splenic weight were found among mice which had been treated with Indomethacin in comparison to PBS-treated mice. According to our results, treatment with prostaglandin inhibitory drugs stimulates murine hemopoietic stem cell proliferation and enhances stem cell recovery following irradiation.
Recurrent anuria in severe hypercapnic acidosis.
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[Schistosomiasis mansoni infestation treated with oxamnaquine].
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[Withdrawal of prolonged corticosteroid therapy].
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Reversible locked-in state in postinfective measles encephalitis.
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Linitis plastica infiltrating the entire gut.
A case of extensive spread of linitis plastica, involving the entire gastrointestinal tract, is reported. The tumor probably originated in the stomach. Because the mucosal and serosal layers remained intact, diagnosis was markedly delayed, as is commonly seen in scirrhous carcinoma. The method of spread of the tumor (mainly through the submucosal layer) is unusual, and is probably related to the histological type of carcinoma.
Myeloblastic metamorphosis in lymph node in a case of chronic myeloid leukemia. A clinical, morphological-ultrastructural and cytogenetic study.
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Hairy cell leukemia: defective production of granulocyte-macrophage colony-stimulating factor by peripheral blood cells.
Granulocyte-macrophage colony-stimulating factor (GM-CSF) production by the peripheral blood (PB) cells of hairy cell leukemia (HCL) patients whose PB contained only 2 to 10% hairy cells was studied in an in vitro bone marrow culture system. In addition, the possible inhibitory effect on the growth of normal granulocyte-macrophage colony-forming cells (GM-CFC) by the patients' mononuclear cells or serum was assayed. GM-CSF production by PB cells of HCL patients was 82 +/- 18% (mean +/- sd) lower than its production by normal PB cells. No significant inhibition of normal GM-CFC growth was observed in the presence of patients' PB mononuclear cells or their serum. These findings suggest that in HCL patients the monocyte-macrophage system is defective in its capacity to produce GM-CSF. This defect may play a role in the impaired granulocyte production known to occur in HCL.
Hypophyseal gonadotropin insufficiency in a young woman with idiopathic hemochromatosis.
A 24-year-old women suffering from primary sterility was diagnosed in 1971 as having idiopathic hemochromatosis (IH). The diagnosis was made on the basis of high serum iron and high transferrin saturation, ferrokinetic studies, including iron absorption, liver biopsy showing heavy deposits of iron in the parenchymatous cells, and a family history. Except for slight elevations in the serum transaminases, there were no clinical or laboratory findings of liver pancreatic, myocardial, or dermal involvement by hemochromatosis. Endocrine evaluation revealed gonadotropin insufficiency as the cause of sterility. The patient was treated with periodic phlebotomies for seven years, and the mount of iron withdrawn during that time was calculated to be approximately 27 g. A repeat liver biopsy showed complete disappearance of the iron excess of the fibrotic changes that had been present in 1971. Repeated relevant clinical and laboratory studies did not reveal any pathological findings consistent with hemochromatosis. A complete endocrine evaluation, including stimulatory tests (luteinizing hormone releasing hormone, thyrotropin-releasing hormone, insulin, and metyrapone), disclosed only findings consistent with hypophyseal gonadotropin insufficiency, and these were attributed to iron deposition. It can be assumed that the prolonged treatment with phlebotomies prevented the development of liver, pancreatic, myocardial, or other clinical endocrine disease, but had no effect on the already damaged pituitary. The patient's clinical course followed the pattern recently described in other young patients with IH.
Iron loading and endocrine functions in nontransfused patients with beta-thalassemia intermedia or sickle-cell thalassemia.
Body iron stores and endocrine functions were determined in eight patients with chronic hemolytic anemia who had received only small amounts of blood and no iron preparations. Four patients had beta-thalassemia intermedia (BTI) and four had sickle-cell thalassemia (SCT). Hemoglobin levels and degrees of hemolysis were similar in both groups of patients. The patients with BTI showed clear evidence of iron overload, whereas there was no evidence of iron accumulation in the patients with SCT. The three patients with BTI who had endocrinologic evaluations showed endocrine dysfunctions. Two patients with SCT had no endocrine abnormalities and the other two probably had some degree of primary hypogonadism. Iron overload in patients with thalassemia probably results from excessive intestinal iron absorption and can damage various parenchymal and endocrine organs, even in the absence of an external source of iron.