[Voluntary abortion: new perspectives in local anesthesia]. / Interruption volontaire de grossesse: nouvelles perspectives de l'anesthésie locale.

New perspectives have been envisioned for the TOP instrumental technique, through the utilization of pharmacologic products, whose property is to dilatate the cervix. Misoprostol or mifepristone, when administrated to a patient a few hours before a TOP by uterine suction curettage, enables a dilatation of the cervix in such a way that it allows the surgically induced abortion to be carried out with local anesthesia, under optimal comfort conditions for the patients as well as for the operator.

Lindane (Kwell)-induced aplastic anemia.

Numerous toxic exposures have been implicated in causing aplastic anemia. Thirteen cases of aplastic anemia and 5 cases of other blood dyscrasias, eg, red blood cell aplasia and thrombocytopenia, associated with lindane, have been reported in the literature. However, aplastic anemia secondary to the scabicidal product (lindane [Kwell]) has not been documented, to our knowledge. We present the case of a 21-year-old man with a diagnosis of aplastic anemia, known prolonged exposure to lindane, and documented elevated serum lindane levels. His clinical course is described as well as various defects are explored for the aplasia.

Granulocytic sarcoma: three unusual patients.

This report describes three unusual patients with lesions due to myeloblasts. In one instance, the patient presented with massive adenopathy. The second patient had bone lesions and a pathologic fracture. The third patient, with myelodysplasia, had diffuse skin lesions infiltrated with myeloblasts. These cases fit the diagnostic category of granulocytic sarcoma. Granulocytic sarcoma is a tumor of immature myeloid cells that may involve any site in the body but that most commonly affects the skin, soft tissues, lymph nodes, bone, and periosteum. Lesions can predate leukemia or occur late in an established chronic granulocytic leukemia or acute granulocytic leukemia. The most common presentation occurs late in the course of acute granulocytic leukemia or in chronic granulocytic leukemia as a herald to blastic transformation. Therapy for localized lesions is radiotherapy, which produces prompt shrinkage of the lesions but relapse occurs subsequently. Systemic chemotherapy also produces satisfactory clinical results. In all instances, therapy can only be considered palliative since virtually all patients have a short survival following the appearance of an extramedullary myeloblastic lesion. Recognition of this pathologic entity at an early stage may give us information on the best management for these patients.

Prolonged unmaintained remission after intensive consolidation therapy in adult acute nonlymphocytic leukemia.

Thirty-five adults with acute nonlymphocytic leukemia who were in complete remission after initial induction therapy received a single course of high-dose cytarabine and amsacrine as consolidation therapy. No further therapy was administered. Despite substantial toxicity, the median duration of disease-free survival was 12 months, and 30% of patients are projected to be alive in continuous complete remission at 3 years. A single course of intensive postremission chemotherapy provides long-term disease-free survival in the absence of any further treatment.

Acute lymphoblastic leukemia of Burkitt's type (L-3 ALL) lacking surface immunoglobulin and the 8;14 translocation.

A 25-year-old man developed acute lymphoblastic leukemia, morphologically of Burkitt's type (L3-ALL, F.A.B. classification) but with immunologic and cytogenetic features not previously reported. The leukemic blasts were B1+, CALLA+, OKT3-, and OKT11-. Surface immunoglobulin and cytoplasmic IgM were not detected, but cytoplasmic IgG lambda was present. Karyotypic analysis of 20 metaphases was normal at presentation but abnormal after relapse. At that time, the predominant karyotype was 47XY, 1q-, 7q-, 12p-, M1. This case illustrates the following: (1) Burkitt cell morphology may accompany some uncommon pre-B-cell lymphoblastic leukemias, and (2) rearrangements involving chromosomes 14, 2 or 22 may not be found in all cases of L-3 ALL.

Evidence for reduced erythroid burst (BFUE) promoting function of T lymphocytes in the pure red cell aplasia of chronic lymphocytic leukemia.

T cells stimulate the proliferation of BFUE (burst forming units-erythroid) from normal blood null cells in an in vitro culture system in the presence of erythropoietin. To determine whether abnormal BFUE proliferating effect of T cells could explain the pure red cell aplasia in chronic lymphocytic leukemia (CLL-PRCA), we investigated the erythropoietic function of T and null cells in four patients with CLL-PRCA and compared results to three patients with idiopathic pure red cell aplasia (I-PRCA) and normals. Sera from I-PRCA patients (P greater than 0.05) but not CLL-PRCA patients (P less than 0.1) inhibited erythroid stem cell proliferation in the presence of complement. BFUE in null cells of all PRCA patients were barely detectable or absent (P less than 0.0025). Normal or I-PRCA T cells increased BFUE proliferation from PRCA null cells of six patients (P less than 0.001). In contrast, CLL-PRCA T cells were poor stimulators of BFUE from autologous (P less than 0.001) or allogeneic null cells (P less than 0.02). Treatment with cyclophosphamide and prednisone induced reticulocytosis in all four CLL-PRCA patients. After treatment, in two cases, the burst promoting function of T lymphocytes was normal. Analysis of T cell subpopulations in two CLL-PRCA patients, suggested that the reduced burst promoting function was due to decreased numbers and/or function of T cells bearing Fc receptors for IgM (TM cells). These findings suggest that reduced generation of a burst promoting activity by CLL-PRCA T cells may contribute to the pathogenesis of PRCA in chronic lymphocytic leukemia.

Chronic granulocytic leukemia following successful renal transplantation.

The use of immunosuppressive therapy has markedly increased over the past several years, and concomitant with its use has been an increased frequency of associated neoplasia. The patient presented is a 22-year-old white male who, following two renal transplants and prolonged immunosuppressive therapy with azathioprine and methylprednisolone, developed chronic granulocytic leukemia. Chromosome karyotyping demonstrated the somewhat unusual development of a Philadelphia chromosome with translocation to the No. 7 of the C group. A review of transplantation centers revealed that five cases of chronic granulocytic leukemia have occurred in a population of 25,000 renal transplant patients, a 5-fold increased incidence over the general population. Possible etiologies that may be responsible for the development of chronic granulocytic leukemia in patients on immunosuppressive therapy are discussed. It is our hope that by the introduction of these reports of chronic granulocytic leukemia into the medical literature, the need for caution in the use of immunosuppressive drugs in nonmalignant disease will again be emphasized.

Plateletpheresis in the management of thrombocytosis.

Acute thrombotic and hemorrhagic manifestations of thrombocytosis associated with myeloproliferative disorders may be life threatening. Conventional therapy with radioisotopes and/or cytotoxic drugs may require weeks for effective control of platelet counts. In five patients, plateletpheresis by discontinuous-flow (Haemonetics) or continuous-flow (Aminco Celltrifuge) centrifugation was used as a means of reducing platelet counts acutely. With each procedure, approximately 2-9 X 10(12) platelets were removed, resulting in decrements in platelet counts and relief of symptoms. Plateletpheresis is a useful and safe acute means of controlling platelet counts in myeloproliferative disorders.

Heparin-induced immune thrombocytopenia.

We studied five patients in whom severe thrombocytopenia developed during intermittent intravenous heparin treatment of arterial and venous thrombosis. Platelet aggregation was demonstrated when heparin (0.5 U per milliliter) was incubated with the patients' citrated platelet-rich plasma or with normal platelet-rich plasma in the presence of the patients' serum. Antiplatelet antibody was not detected in the patient globulin fractions prepared from serum collected within one week after heparin withdrawal by use of the platelet factor 3 availability technic. When the studies were repeated with modifications to detect heparin-dependent antiplatelet antibodies, positive results were obtained in four of five patients. The data suggest that a casual relation, mediated by an immune mechanism, existed between heparin therapy and thrombocytopenia, and that this syndrome may occur more often than has previously.