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PubMed2002

Leukopenia and thrombocytopenia in hemodialysis patients with hepatitis B or C virus infection and non-hemodialysis patients with hepatitis cirrhosis.

AIMS: To investigate the relation of leukopenia and thrombocytopenia in hemodialysis (HD) patients with hepatitis C virus (HCV) infection. MATERIALS AND METHODS: The study included 86 HD patients with hepatitis B surface antigen-negative and hepatitis C antibody-negative, 28 HD patients with hepatitis C antibody-positive, 22 HD patients with hepatitis B surface antigen-positive, 78 non-HD patients with hepatitis B-induced liver cirrhosis and 38 non-hemodialysis patients with hepatitis C-induced liver cirrhosis. The following parameters were checked: anti-HCV, hepatitis B surface antigen, hemoglobin, hematocrit, white blood cells, platelets, calcium, phosphate, iron, ferritin, albumin, globulin, aspartate transaminase (AST), alanine transaminase (ALT) and C-reactive protein. The history of blood transfusions, medications, erythropoietin doses and adequate dialysis (KTNV) for 6 consecutive months was also recorded from charts. RESULTS: The HD patients with positive serum anti-HCV and non-HD patients with hepatitis B- or C-induced liver cirrhosis had higher prevalences of leukopenia (39.3%, 43.6% and 50% vs. 15.1%; p < 0.001) and thrombocytopenia (67.9%, 89.7% and 81.6% vs. 34.9%: p < 0.001) than HD patients with serum anti-HCV(-)HbsAg(-). The WBC (4,432 +/- 1,394, 4,792 +/- 2,263 and 4,624 2,446 vs. 5,590 +/- 1,500/mm3; p < 0.001) and platelet counts (140 +/- 45, 80 +/- 50 and 89 +/- 65 vs. 186 +/- 62 x 10(3)/mm3; p < 0.001) of HD patients with positive serum anti-HCV and non-HD patients with hepatitis B- or C-induced cirrhosis were also lower than HD patients without anti-HCV antibody. The liver cirrhosis patients had more thrombocytopenia than the HD patients with anti-HCV(+). The WBC and platelet counts did not vary between HD patients with HbsAg(+) and HD patients with anti-HCV(-)HBsAg(-). The durations of HD, hepatitis and liver cirrhosis were not related to the leukopenia or thrombocytopenia (p > 0.05). CONCLUSIONS: HCV infection associated with leukopenia and/or thrombocytopenia in HD patients is as common as in non-HD patients with liver cirrhosis. This may be due to the direct effect of hemopoiesis rather than the hyperspleenism of liver cirrhosis patients. There is a need for further prospective investigation to ascertain the clinical significance of leukopenia and thrombocytopenia in HD patients with anti-HCV(+). The prevalence of leukopenia and thrombocytopenia was higher in HD patients with hepatitis C than in HD patients with hepatitis B and HD patient without hepatitis.

Adult↗
PubMed1987

Leukopenia secondary to silver sulfadiazine: frequency, characteristics and clinical consequences.

Leukopenia associated with silver sulfadiazine (SSD) is a frequent event and may be a risk factor for infectious complications in the burn patient. This study reviews 77 patients with thermal injuries to determine total body surface area (BSA) burned, and white blood cell count (WBC) at time of hospital admission. A subpopulation of 56 patients with serial WBC counts were evaluated to determine lowest WBC count, topical burn therapy, episodes of infection or septic shock and final outcome. There was not a significant incidence of leukopenia on admission. Fifty-six per cent of patients treated with SSD and 12 per cent of silver nitrate-treated patients became leukopenic (P less than .05). The leukopenia was higher among SSD-treated patients who had greater than 15 per cent BSA burns (P less than .05). The onset of leukopenia generally occurred the second day after the burn and the WBC count returned to normal with discontinuance of the drug. The leukopenia was due primarily to a marked decrease in the number of mature neutrophils. There was no difference in the incidence of septic complications or opportunistic infections in the treatment groups. There was no significant difference in final outcome. Silver sulfadiazine-induced leukopenia appears to be a self-limited phenomenon that does not increase the incidence of infectious complications nor affect final outcome.

Adolescent↗
PubMed1978

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↗
PubMed1998

[Use of filgrastim, granulocyte colony stimulating factor (G-CSF), in radiotherapy to reduce drop-outs because of radiogenic leukopenia].

Radiotherapy patients are at risk of developing leukopenia, which risk depends on the irradiated volume, the rate of irradiated bone marrow and the radiation dose. Radiogenic leukopenia may cause radiotherapy drop-out, with consequent effects, on local tumor control and clinical outcome. The introduction of granulocyte growth factors, such as filgrastim, has permitted to accelerate normal neutrophil count recovery in irradiation-related neutropenia both in vitro and animal models; clinical experience in humans is still lacking, relative to both indications and scheduling. In the Oncologic Radiotherapy Department of Treviso Hospital, 31 patients irradiated for Hodgkin disease, rectal cancer and other malignancies, who presented leukopenia requiring treatment discontinuation, were given filgrastim to assess its actual effect in avoiding further drop-outs and to compare two administration schedules (2 or 3 vials, 30 MIU, weekly). Filgrastim treatment was continued throughout the radiotherapy cycles, for 1 to 5 weeks. Eighteen patients had received previous chemotherapy and 11 were undergoing concurrent 5-fluorouracil chemotherapy-irradiation. A mean 203% increase in leukocyte count was observed (136% in the patients treated with 2 vials/week and 274% in those receiving 3 vials/week); this increase was more apparent in women that in men (256% versus 91%) and slightly higher in patients 50 years old and with target volumes < 5000 ml. Filgrastin treatment was well tolerated by all patients, with no discontinuations due to adverse effects; 9 patients (29%) reported skeletal pain, which was marked in 2 of them only. Eighty percent of patients completed all the radiotherapy cycles with no discontinuation, while 6 patients dropped out because leukopenia persisted. Biweekly filgrastim administration was effective to prevent unscheduled radiotherapy discontinuation in 75% of patients and triweekly administration was effective in 86% of patients. In our experience, filgrastim administration was well tolerated and effective in decreasing the irradiation drop-outs caused by treatment-related leukopenia. Since this drug is rather expensive, we decided to use routinely the lower dosage of biweekly administration (with one vial given on Friday and Saturday, to permit neutrophil recovery during the day off) and to reserve the higher dosage (3 vials a week) to the patients with large body areas, big target volumes and persistent leukopenia during previous chemotherapy.

Adolescent↗
PubMed1998

Incidence of leukopenia and cytomegalovirus disease in kidney transplants treated with mycophenolate mofetil combined with low cyclosporine and steroid doses.

Mycophenolate mofetil (MMF) combined with conventional cyclosporine and steroids doses efficiently prevents acute rejection in kidney transplants. However, this regimen has been associated with an increased incidence of cytomegalovirus (CMV) disease and leukopenia, specially in patients receiving MMF at 3 g/d, suggesting that the combination of two powerful immunosuppressants carries the risk of overimmunosuppression. For this reason, we treated a group of patients with MMF 3 g/d combined with low cyclosporine and steroids doses. Eighty-two kidney transplants performed at two centers and enrolled in the European Mycophenolate Mofetil Cooperative Study were randomized to receive: A) placebo (n = 27); B) MMF 2 g/d (n = 27); and C) MMF 3 g/d (n = 28). In this double blind study all patients received cyclosporine and steroids at conventional doses. Fifteen kidney transplants enrolled in an MMF open pharmacokinetic study were treated with MMF 3 g/day combined with low cyclosporine and steroid doses (group D). Efficacy was evaluated as the incidence of biopsy proven acute rejection, and safety focused on CMV disease and leukopenia. Patients receiving MMF showed a low incidence of biopsy proven rejection (B) 18.5%; C) 10.7%; and D) 13.3%). Patients of group C had a high incidence of CMV disease (35.7%) when compared with the other groups (lower than 8%). Incidence of leukopenia was higher in patients treated with MMF (B) 25.9%; C) 39.3%; and D) 40%) than in placebo treated patients (7.4%). Patients in group (C) displayed leukopenia mainly in the context of CMV disease, while patients of group (D) had leukopenia not related to CMV infection. All patients of group (D) who presented leukopenia recovered after MMF reduction dose, while in group (C) there were 5 out of 28 patients who required MMF withdrawal. We propose that a reasonable approach to take advantage of a powerful non-nephrotoxic immunosuppressant such as MMF, could be the administration of this drug at 3 g/d from the time of transplantation combined with low CsA and steroid doses.

Adult↗
PubMed1982

Cyclophosphamide-induced leukopenia and suppression of limb regeneration in the adult newt, notophthalmus viridescens.

Cyclophosphamide (cytoxan), a clinical immunosuppressant, produced a marked, persistent leukopenia (greater than 40% reduction) in adult newts in contrast to a transient, milder leukopenia accompanying amputations without cytoxan treatments. In addition, cytoxan suppressed the formation of regeneration blastemata initially: however, blastema formation occurred if a second amputation was performed two or more weeks following the cessation of cytoxan treatments. The failure of the leukopenias of these latter cases to be corrected suggests that although a cytoxan-induced leukopenia is correlated with the absence of forelimb regeneration, this leukopenia is not, of itself, a sufficient condition to inhibit regeneration.

Animals↗
PubMed1989

Influence of leukopenia on collateral flow, reperfusion flow, reflow ventricular fibrillation, and infarct size in dogs.

Leukocytes contribute to myocardial damage during ischemia and reperfusion. However, the mechanism involved has not been clearly elucidated. The purpose of the present study was to determine whether leukocyte-induced myocardial damage is flow mediated. In open-chest dogs submitted to 2 hours of ischemia, area at risk, infarct size, and regional myocardial blood flow before, during, and after ischemia were measured. Leukopenia was induced by a two-step method (chemotherapy and antineutrophil serum) in a group of 14 dogs as compared to a control group of 18 dogs. The relation of infarct size to the major determinants of infarct size was analyzed by uni- and multilinear regressions. Seven control dogs had ventricular fibrillation at reperfusion compared to one dog with leukopenia. In the group with leukopenia the mean infarct size was smaller (31.1 +/- 5.8% of area at risk) than in the control group (47.7 +/- 2.9, p = 0.02). In addition, the two multiple linear regression equations were significantly different (p = 0.01). Myocardial blood flow to the central ischemic zone did not change significantly between 20 and 120 minutes of ischemia in the control dogs (n = 12; subendocardial = 0.08 +/- 0.03 vs 0.07 +/- 0.03 ml/min/gm; subepicardial = 0.20 +/- 0.07 vs 0.20 +/- 0.05 ml/min/gm) and in the dogs with leukopenia (n = 12; 0.07 +/- 0.02 vs 0.07 +/- 0.02 ml/min/gm and 0.15 +/- 0.004 vs 0.18 +/- 0.04 ml/min/gm). A similar reduction in myocardial blood flow was observed after 6 hours of reperfusion in the control dogs (0.34 +/- 0.07 ml/min/gm vs 1.02 +/- 0.11 at baseline, p less than 0.01) and in the dogs with leukopenia (0.25 +/- 0.04 vs 0.81 +/- 0.08 ml/min/gm, p less than 0.01). It was concluded that the leukocyte-dependent myocardial injury did not appear to be mediated through a flow mechanism during either ischemia or reperfusion.

Animals↗
PubMed1980

Leukopenia, hypoxia, and complement function with different hemodialysis membranes.

Complement activation during exposure of plasma to cuprophan has been postulated to cause leukopenia and hypoxia in hemodialysis patients. To determine if hypoxia is related to leukopenia and if complement activation leads to a depletion of functional complement components, we dialyzed four patients three times sequentially against each of four types of membranes: cuprophan, regenerated cellulose, cellulose acetate, and polyacrilonitrile. Within 20 min there was a marked leukopenia with cuprophan from 5541 +/- 376 to 1216 +/- 94 (P less than 0.001) and with regenerated cellulose from 5541 +/- 411 to 1533 +/- 203 (P less than 0.001). With cellulose acetate, the change from 5558 +/- 400 to 3783 +/- 341 (P less than 0.001) was less dramatic, and with polyacrilonitrile the fall from 5591 +/- 381 to 464 +/- 401 (P less than 0.02) was minimal. After 2 and 4 hours of dialysis, a rebound leukocytosis was seen with cuprophan, regenerated cellulose, and cellulose acetate, but not with polyacrilonitrile. Transient thrombocytopenia occurred with cuprophan and regenerated cellulose. In spite of the variable degree of leukopenia, all membranes induced a similar and significant hypoxia, which was progressive throughout dialysis, even during the rebound leukocytosis. After 4 hours, the mean PO2 ranged from 91 to 93 mm Hg with all membranes. Functional hemolytic titers of whole complement, C3, C5, and C4 were normal prior to hemodialysis and failed to decrease after 4 hours with any membrane. It is concluded that hemodialysis leukopenia is membrane-dependent and is not the cause of hypoxia. In addition, hemodialysis complement activation does not lead to functional complement depletion and is of no clinical significance.

Adult↗
PubMed2003

[Clinical application of Lishengsu for treatment of leukopenia induced by chemotherapy].

The efficacy and safety of Lishengsu (a rhG-CSF preparation) were evaluated for treatment of chemotherapy-induced leukopenia. 327 cases of leukopenia with grade I-IV induced by chemotherapy were subcutaneously administered at 2.5 - 5.0 micro g/(kg x d) of Lishengsu, and hemogram and the side effects were observed. The results showed that Lishengsu had satisfactory effect to cure leukopenia after chemtherapy, with an effective rate of 99.4% (325/327), the side effects were quite slight. It is concluded that Lishengsu is efficient and safe for patients with leukopenia, and can be used as an adjuvant drug for treatment of leukopenia after chemotherapy.

Adolescent↗
PubMedDate not supplied

Mortality, major amputation rates, and leukopenia after isolated limb perfusion with phenylalanine mustard for the treatment of melanoma.

BACKGROUND: Isolated limb perfusion (ILP) is a treatment for cutaneous melanoma performed by several centers worldwide. The final data analysis of the World Health Organization and European Organization for Research and Treatment of Cancer in the use of ILP as adjuvant treatment for cutaneous melanoma is pending. ILP is effective to treat recurrent cutaneous melanoma. We determined the published rates of morbidity and mortality of ILP and put that component of the procedure into contemporary perspective. METHODS: A MEDLINE search was conducted of the English-language literature from 1980 to 1995 for all publications reporting perfusion with phenylalanine mustard alone or combined with other agents. Patients treated by staged perfusion or fractional doses of chemotherapy were excluded. All published series were analyzed for the rate of mortality, number of major amputations, and presence of leukopenia. RESULTS: The 30-day mortality rate for > 2,000 patients was 0.6%. Death often resulted from cardiopulmonary complications or overwhelming sepsis from leukopenia. Leukopenia occurred in 0.7% of patients reviewed, caused by leakage of chemotherapeutic agents into the systemic circulation. Major amputations occurred in 0.8% of patients, and most were of the lower extremity. CONCLUSIONS: The definition of efficacy of ILP in the treatment of extremity melanomas remains to be clearly defined. However, based on this review of worldwide publications, the risk of death, amputation, and leukopenia is low.

Amputation, Surgical↗
PubMed2006

Prolongation of clozapine-induced leukopenia with olanzapine treatment.

Clozapine is a well-known antipsychotic to cause fatal agranulocytosis but there are only a few case reports about the risk of leukopenia and agranulocytosis associated with other atypical antipsychotics. Olanzapine has structural pharmacological similarities to those of clozapine and reports about haematological adverse effects of olanzapine include three groups: the first group includes cases of olanzapine-induced neutropenia, the second informing that olanzapine is safe after clozapine induced agranulocytosis and the third group forms prolongation of clozapine-induced leukopenia with olanzapine use. The aim of this paper is to report a case of prolongation of clozapine-induced leukopenia despite olanzapine treatment and discuss leukopenia caused by atypical antipsychotic use in the light of recent and limited literature.

Adult↗
PubMed1999

Massive blood transfusion exceeding 50 units of plasma poor red cells or whole blood: the survival rate and the occurrence of leukopenia and acidosis.

The survival rate after bleeding requiring massive blood transfusions exceeding 50 units has been reported to be low or zero. There seems to be no reports of leukopenia in connection with massive blood transfusion. This retrospective study was carried out to investigate the survival rate and the occurrence of leukopenia and acidosis in patients who were transfused with more than 50 units of plasma poor red cells or whole blood. The survival rate was 16 of 23. Three of the five patients with a blood transfusion of over 100 units survived. Pure component therapy was used on 18 occasions. All patients had a leukopenia, which lasted up to five days. All patients had an acidosis. The range of the lowest pH values in patients who did not survive was from 6.77 to 7.27 and in survivors from 6.87 to 7.28. The survival rate was considerably higher than reported in previous studies. Pure component therapy appeared to be particularly suited to massive transfusion. Leukopenia was a regular phenomenon. Severe acidosis did not predict a poor outcome.

Acidosis↗
PubMed1996

Comparison of two strategies for the treatment of radiogenic leukopenia using granulocyte colony stimulating factor.

PURPOSE: Radiation-induced leukopenia can cause a delay or discontinuation of radiotherapy. This complication can be overcome with the use of granulocyte colony-stimulating factor (G-CSF). However, an uncertainty exists regarding the mode of application of G-CSF in patients treated with radiotherapy. For this reason, the efficacy of two strategies for the administration of G-CSF in irradiated patients was compared in a prospective randomized clinical study. METHODS AND MATERIALS: Forty-one patients who developed leukopenia (< 2.5 x 10(9) per liter) while undergoing radiotherapy were treated with G-CSF at a daily dose of 5 microg/kg. The first group received single injections of G-CSF as required (n = 21). The second group received G-CSF on at least 3 consecutive days (n = 20). An analysis was made of the changes in leukocyte counts, the number of days on which radiotherapy had to be interrupted, and the side effects of growth-factor treatment. RESULTS: An increase in leukocyte values in the peripheral blood was observed in all patients treated with G-CSF. In the group which received G-CSF when required, two injections (range: 1-8) were administered in most cases. In the second group, most of the patients received three injections (range: 3-9). The average duration of therapy interruptions due to leukopenia was 4.8 days (0-28) in the first therapy arm and 2.5 (0-20) in the second arm. The variance in the duration of therapy interruptions between the two groups was not significant (p = 0.2). Radiotherapy had to be terminated in two patients due to thrombocytopenia but the application of G-CSF did not seem to be a reason of decreasing platelet counts. CONCLUSIONS: Our results reveal that G-CSF is safe and effective in the treatment of radiation-induced leukopenia regardless of the mode of application. Because the calculated difference related to radiation treatment interruptions has no clinical relevance, both approaches examined in our study appear reasonable.

Adult↗
PubMed1983

Hemodialysis leukopenia and complement function with different dialyzers.

The relationship between leukopenia and the complement system during hemodialysis was re-examined by studying not only the in vivo effects of four different dialyzer membranes (cellulose hydrate, cuprophan, cellulose acetate, and polyacrilonitrile) on leukocyte counts and complement levels, but especially by investigating the effects of these membranes on complement function in vitro. Whereas from in vivo studies no definite conclusions could be drawn, in vitro investigations provided clear-cut information. When more sophisticated technical approaches were undertaken, it became evident that hemodialysis leukopenia has to be thought of in terms of chemotactic factor generation. In fact, a strict correlation was demonstrated between the degree of leukopenia induced by the dialyzers tested and the ability of the relative membrane to generate chemotactic activity in vitro. Moreover, the previously observed ability of polyacrilonitrile membrane to induce a decrement in complement function was due to the ability of polyacrilonitrile to adsorb complement activity and did not correspond to effective complement consumption. This finding explained why polyacrilonitrile dialysis is not accompanied by a decrease in circulating granulocytes. Taken together, our data strongly point to a pivotal role of complement system in the pathogenesis of hemodialysis leukopenia.

Acrylic Resins↗
PubMed1999

Omeprazole-induced leukopenia. A case report.

BACKGROUND: Omeprazole has been marketed in France since 1989, for the healing of peptic ulcers, erosive reflux oesophagitis, and the Zollinger-Ellison syndrome. However, the drug has been associated with serious adverse reactions, including haemolytic anaemia and acute interstitial nephritis. More recently, an autoimmune syndrome induced by omeprazole has been described. OBJECTIVE: We present here a clinical history and an in vitro test of cytotoxicity linking leukopenia to omeprazole. RESULTS: A 37-year-old woman was hospitalized in the intensive care unit of our hospital with acute pulmonary insufficiency secondary to pneumonia. 72 h after starting omeprazole treatment, a decrease in leucocyte count was observed. The leukopenia was maximal on day 22: total white cell count was 2. 1x109/l, and neutrophil count was less than 0.75x109/l. In order to find the cause of this leukopenia, an in vitro cytotoxicity test was performed. The test was positive only when patient neutrophils and patient serum were in the presence of omeprazole. This cytotoxicity seems to be complement-dependent, as in the presence of heated serum, the omeprazole toxic effect was substantially reduced. CONCLUSION: This case report suggests that the leukopenia was associated with omeprazole.

Adult↗
PubMedDate not supplied

Leukopenia in acute thermal injury: evidence against topical silver sulfadiazine as the causative agent.

White blood cell data from time of admission to 4 days after burn injury was retrospectively reviewed to determine differences in the incidence of leukopenia in patients with burn injuries treated topically with either silver sulfadiazine or silver nitrate. WBC counts decreased in both groups of patients during the first 3 days after burn injury. An incidence of leukopenia (WBC count less than or equal to 5000/mm3) was observed in of 40 (47.5%) patients treated with silver sulfadiazine and in 13 of 30 (43.3%) patients treated with silver nitrate. There was no statistical difference in the incidence of leukopenia between the two treatment groups. These data suggest that silver sulfadiazine may not be the cause of the leukopenia observed early after burn injury.

Administration, Topical↗
PubMed2001

Dose-dependent olanzapine-associated leukopenia: three case reports.

Leukopenia and agranulocytosis are well reported and dangerous haematological side-effects associated with the use of typical and atypical antipsychotics. These potentially life-threatening phenomena have led to treatment discontinuation and the consequent reemergence of psychiatric symptoms. We report three cases of patients who developed leukopenia during olanzapine treatment. In each case, the leukopenia was dose-dependent. Reduction in the dose of olanzapine was followed by normalization of the white blood count which allowed continuation of the medication. These cases suggest the possibility that, in some patients, leukopenia or agranulocytosis during olanzapine treatment might be dose-related. Thus, olanzapine dose reduction may permit treatment continuation where this is clinically indicated. In our cases, haematological side-effects were satisfactorily controlled by dose reduction without allowing the reemergence of psychiatric symptoms. This clinical management may offer an alternative to treatment suspension. A careful monitoring of the white blood count is obviously recommended. Olanzapine may be considered a potential and safer treatment for a this specific group of patients.

Adolescent↗
PubMed1982

Leukopenia and silver sulfadiazine.

The relationship of silver sulfadiazine therapy to leukopenia has been controversial. In our burn unit the incidence of leukopenia increased dramatically in 1978. Leukopenia was observed only in silver sulfadiazine-treated patients and not in patients treated with other agents. Because cimetidine had been introduced at about that time, the possibility of a drug interaction was investigated with a prospective randomized study. It was found that leukopenia continued to appear in a large percentage of patients in both groups, although the incidence was higher in cimetidine-treated patients.

Adult↗