[Leukopenia and lymphopenia during the radiation therapy and their recovery by anti-leukopenia drugs (author's transl)].
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Alkaloids↗
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Results for “Leukopenia”
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Familial leukopenia among Yemenite Jews.
Benign familial leukopenia was found in 75 of 200 healthy Yemenite Jews examined. The leukopenia was not a constant finding and was not associated with a tendency toward infection. HLA typing showed no significant differences in the frequency of the various HLA antigens between the subjects with and without leukopenia. No similarity was found between the HLA of the Yemenite Jews with leukopenia and that reported in black Africans with benign familial leukopenia. The suggestion of a genetic contribution from African blacks to Yemenite Jews is not supported by these results. The question remains to be answered whether the familial leukopenia in Yemenite Jews and black Africans is the result of a mutation.
Adolescent↗
Frequency of leukopenia incidents following azathioprine therapy after kidney transplantation.
The frequency of leukopenia incidents and its dependence on the dose of azathioprine and kidney function were analyzed in 149 patients during the first 3 months after kidney transplantation. The results were compared with the data of 42 transplantation centers of the world. We found that the frequency of leukopenia increases significantly following azathioprine dosage exceeding 1.99 mg/kg body weight/day. The toxicity of the drug depends on the kidney function. Most of the leukopenia incidents were detected during the first 5 weeks after kidney transplantation. In 70% of the cases a first leukopenia incident is followed by a second. Low azathioprine dosage after the first episode diminishes the number of second incidents.
Azathioprine↗
Leukopenia and hypoxemia. Unrelated effects of hemodialysis.
Hemodialysis-induced hypoxemia has been attributed to membrane-related complement activation leading to pulmonary leukostasis and to hypoventilation secondary to carbon dioxide losses via the dialyzer. We have separately assessed the role of membrane- and dialysis-related factors by using different dialyzers and sequential ultrafiltration and hemodialysis with first-use cellulose dialyzers produced both leukopenia and hypoxemia. With reused cellulose and polyacrylonitrile dialyzers, hypoxemia still occurred, but without leukopenia. Ultrafiltration produced leukopenia and no changes in Pao2; during the subsequent hemodialysis, hypoxemia developed as the leukocyte count increased by 50%. Our data indicate that leukopenia and hypoxemia are unrelated effects of hemodialysis, and favor hypoventilation as the major determinant of hypoxemia during hemodialysis.
Adult↗
Leukopenia and granulocytopenia after oxacillin therapy.
Two cases of granulocytopenia and leukopenia developing after high-dosage oxacillin therapy given intravenously are described. One patient developed leukopenia and granulocytopenia after 17 days of therapy. The conditions were reversible when oxacillin therapy was discontinued. In the other case, the adverse reaction developed within 48 hours after therapy began and the patient died from heart failure. Leukopenia and granulocytopenia as adverse effects of oxacillin therapy should be kept in mind, especially when high dosages are used.
Adolescent↗
Leukopenia due to penicillin and cephalosporin homologues.
Leukopenia is an infrequently recognized complication of penicillin-related antibiotic and cephalosporin therapy. We describe our experience with nine individuals and reviewed reports of 11 cases from the literature. Seventy-six percent of cases occurred in individuals receiving 150 mg/kg/day or more of the various penicillin and cephalosporin homologues; 67% received these high doses for two or more weeks before the onset of leukopenia. Leukopenia was unusual within the first week of antibiotic treatment. Standard medical texts often recommend blind administration with 12 to 23 g/day of these antibiotics regardless of weight. It is suggested that these antibiotics be administered according to a maximum milligram per kilogram per day dosage as is done in children. Beyond the first week of administration, careful monitoring of the blood cell count should be conducted for those receiving high doses of these antibiotics.
Adolescent↗
Leukopenia in anorexia nervosa. Lack of increased risk of infection.
To determine whether patients with anorexia nervosa (AN) and leukopenia have an increased risk of infection, we reviewed the incidence of leukopenia and infection in 68 cases of AN and studied the mechanism of profound neutropenia in one. Compared with controls, patients with AN had substantially lower total leukocyte counts and absolute neutrophil, lymphocyte, and monocyte counts. Despite frequent and often severe panleukopenia, the patients with AN had no more infections than did the control subjects. The patient with severe neutropenia ahd a hypocellular bone marrow biopsy specimen showing relative myeloid hyperplasia, normal distribution of neutrophils between the marginal and circulating pools, and normal bone marrow neutrophil reserves as estimated by response to hydrocortisone sodium succinate. We conclude that patients uith AN and associated leukopenia do not have increased infection propensity.
Adolescent↗
Acute leukopenia during topical burn therapy with silver sulfadiazine.
Leukopenia, with a mean white blood cell count of 2,680/mm3, was observed in nine patients with thermal injury early in the course of topical treatment with silver sulfadiazine. All manifested absolute neutropenia with a concomitant increase in immature band forms in the peripheral blood smear. The leukocyte counts returned to within normal limits within 48 to 72 hours of discontinuation of silver sulfadiazine therapy in four patients, and also did so in five patients in whom silver sulfadiazine therapy was continued. Leukopenia secondary to silver sulfadiazine application is currently believed to be an innocuous, self-limited phenomenon.
Acute Disease↗
Acute leukopenia associated with silver sulfadiazine therapy.
A patient with a 30% scald burn was treated with topical silver sulfadiazine (Silvadene). On two occasions, within 48 hours of treatment, the patient developed acute leukopenia. Bone marrow aspiration revealed cell maturation arrest. The possible mechanisms of this leukopenia are discussed. It is recommended that daily leukocyte counts be done in burn patients being treated with silver sulfadiazine.
Acute Disease↗
Severe leukopenia secondary to carbamazepine administration.
We have reported the first case of severe leukopenia, complicated by infection, associated with the use of carbamazepine. In the literature, most cases of leukopenia secondary to carbamazepine are transient and benign, but any increase in dosage of the drug warrants a close follow-up of blood counts even if previous blood counts were normal.
Adult↗
Acceleration of myeloid recovery from cyclophosphamide-induced leukopenia by pretreatment with Bacillus Calmette-Guérin.
Treatment of C57BL/6 mice with Bacillus Calmette-Guérin i.p. 8 days prior to the induction of leukopenia by cyclophosphamide (300 mg/kg i.p.) significantly (p less than 0.002) increased peripheral granulocyte counts on each day during the recovery from leukopenia. The recovery of lymphocyte counts was unaffected by Bacillus Calmette-Guérin treatment. Further experiments indicated that the accelerated granulocyte recovery was the result of an earlier initiation of the recovery process rather than of the release of stored granulocytes. Bacillus Calmette-Guérin may have clinical value as a stimulator of myelopoiesis in patients rendered leukopenic by antineoplastic chemotherapy.
Animals↗
Hemodialysis leukopenia. Pulmonary vascular leukostasis resulting from complement activation by dialyzer cellophane membranes.
Acute leukopenia occurs in all patients during the first hour of hemodialysis with cellophanemembrane equipment. This transient cytopenia specifically involves granulocytes and monocytes, cells which share plasma membrane reactivity towards activated complement components. The present studies document that complement is activated during exposure of plasma to dialyzer cellophane, and that upon reinfusion of this plasma into the venous circulation, granulocyte and monocyte entrapment in the pulmonary vasculature is induced. During early dialysis, conversion of both C3 and factor B can be demonstrated in plasma as it leaves the dialyzer. Moreover, simple incubation of human plasma with dialyzer cellophane causes conversion of C3 and factor B, accompanied by depletion of total hemolytic complement and C3 but sparing of hemolytic C1. Reinfusion of autologous, cellophane-incubated plasma into rabbits produces selective granulocytopenia and monocytopenia identical to that seen in dialyzed patients. Lungs from such animals reveal striking pulmonary vessel engorgement with granulocytes. The activated complement component(s) responsible for leukostasis has an approximate molecular weight of 7,000-20,000 daltons. Since it is generated in C2-deficient plasma and is associated with factor B conversion, it is suggested that activation of complement by dialysis is predominantly through the altermative pathway.
Adult↗
Leukopenia-induction capacity of 6-MP metallo-purine complexes in the rat.
Six-MP and its palladium and platinum complexes of this compound were administered intraperitoneally to 28 day old Sprague-Dawley rats in dosages of 15 mg/kg, 26.85 mg/kg, respectively for 21 days. The leukopenia induction capacity of 6-MP was greater at the end of day 7 while the 6-MP-Pd complex evidenced a more drastic leukocyte reduction at the end of day 21. The platinum complex was less toxic, as demonstrated by greater weight gain, while treatment with the palladium complex resulted in approximately the same weight gain as that observed in rats treated with pure 6-MP.
Animals↗
Hemodialysis leukopenia and polymorph random mobility-a possible correlation.
In vitro studies of polymorphs exposed to cellulose and polysulfone membranes showed severe impairment in randommobility with the cellulose membrane. In vivo studies with the two membranes showed that profound leukopenia occurred only when cellulose membrane was used. It is suggested that random mobility may have importance in the regulation of peripheral polymorph levels.
Cell Movement↗
Leukopenia after postmastectomy irradiation.
Significant peripheral white blood cell depression was noted in 75% of postmastectomy patients receiving chest wall and nodal irradiation and in 50% of patients receiving only peripheral nodal irradiation. Leukopenia was documented for as long as 36 months following therapy. With the current trend to earlier institution of chemotherapy, the routine use of postoperative irradiation must be reevaluated.
Breast Neoplasms↗
Thrombocytopenia in the absence of leukopenia associated with the use of neuroleptics.
Thrombocytopenia, a fairly uncommon side effect of phenothiazine treatment, usually appears in the presence of a concommitant leukopenia. The authors report 1 patient in whom the illness appeared in the presence of a long known Beta thalassemia but without evidence of alteration in myeloid or lymphoid series. Platelet changes were seen in the presence of a butyrophenone and an aliphatic phenothiazine. A piperazine derivative was used without difficulty.
Adult↗
Association of leukopenia and intestinal permeability with radiation-induced sensitivity to endotoxin.
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Animals↗
Severe combined immunodeficiency with leukopenia (reticular dysgenesis) in siblings: immunologic and histopathologic findings.
The hematologic and histologic features of two, nontwin, male siblings with severe combined immunodeficiency and variable granulocytopenia are compared to the four previously reported cases of reticular dysgenesis. These sibs died at 50 and 3 days of age, respectively, with Pseudomonas sepsis and congenital cytomegalovirus infection, respectively. A maternal uncle has selective IgA deficiency. Cord blood from the second sib contained a normal percentage of E-rosetting lymphocytes; however, these lymphocytes failed to respond to mitogenic stimulation in vitro. Erythrocyte and lymphocyte levels of adenosine deaminase were elevated in the father and the second sib. Serum immunoglobulin concentrations were low in both siblings.
Adenosine Deaminase↗