Effect of leukopenia and leukocytosis on tumor growth and survival time. I. Leukopenia.
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Animals↗
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Effect of experimental leukopenia on chronic gingival inflammation in dogs. 1. Induction of leukopenia by nitrogen mustard.
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Animals↗
The effect of experimental leukopenia on chronic gingival inflammation in dogs. 2. Induction of leukopenia by heterologous anti-neutrophil serum.
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Animals↗
[Leukopenia and lymphopenia during the radiation therapy and their recovery by anti-leukopenia drugs (author's transl)].
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Alkaloids↗
[Leukopenia due to anti-tuberculous chemotherapy including rifampicin and isoniazid].
OBJECTIVES: To examine the incidence rate by age and gender of leukopenia caused by chemotherapy including rifampicin (RFP) and isoniazid (INH), and to study the relationships between the leukopenia and the hepatic side effect or other haematological disorders such as thrombocytopenia. SUBJECTS: Out of the tuberculosis patients who were admitted to our hospital in 1987-88, 1991-92, and 1996-2000, 1,525 patients (1,153 men, 372 women) were chosen for our study who had the white blood cell counts (WBC) in the peripheral blood more than 3,000/mm3 before chemotherapy, and underwent haematologic examination at least twice within 3 months after starting chemotherapy. METHODS: The definition of leukopenia was as follows: 1) WBC became less than 3,000/mm3 during chemotherapy for patients with pre-treatment WBC more than 4,000/mm3, or 2) WBC decreased more than 1,000/mm3 in patients with pre-treatment WBC between 3,000 and 4,000/mm3. The incidence rates of leukopenia by age, gender, and regimens of chemotherapy were calculated. The case-control study was done between the control and the leukopenia groups excluding patients suffered from agranulocytosis to clarify the hematological and biochemical characteristics of the leukopenia group. The control patients were chosen in the following way. For each patient with leukopenia, a patient with the same admission year, same gender, same regimen of chemotherapy, and the nearest age was chosen as a control patient. The changes in counts of white blood cell, granulocyte, and platelet, in hemoglobin concentration, and in hepatic enzyme levels before and during chemotherapy were compared between the leukopenia and the control groups. Thrombocytopenia was defined as platelet count less than 15 x 10(4)/mm3 and hepatic dysfunction as either asparate aminotransferase (AST) higher than 31 IU/l or alanine aminotransferase (ALT) higher than 34 IU/l. RESULTS: (1) Incidence rate of leukopenia The leukopenia appeared in 36 patients (14 men, 22 women), two (one man, one woman) of whom showed agranulocytosis. The incidence rate was 1.2% (14/1,153) for men and 5.9% (22/372) for women. The incidence rate of women was higher than that of men in the age groups between 20 to 79 y.o., but no difference was seen in the age groups elder than 80 y.o. There were no differences in the incidence rate among groups treated with HRE (E: ethambutol), HRS (S: streptomycin), and HREZ (Z: pyrazinamide). The chemotherapy was continued in 30 patients after the appearance of leukopenia, and the natural recovery from leukopenia was seen in 19 patients, while the leukopenic state lasted during the chemotherapy in the remaining 11 patients. In two patients who exhibited agranulocytosis all drugs were discontinued. In the remaining 4 patients one or more drugs were discontinued. (2) Case-control study between leukopenia (N = 34) and the control (N = 34) groups There were no differences in age, sputum culture positivity on admission, degree of roentgenographic extent of the disease, ratio of cavity formation, and quantity of daily doses between the two groups. There was also no difference between the days until leukopenia appeared after starting chemotherapy (47.6 +/- 29.5 days) in the leukopenia group, and the days until WBC count became minimum within 3 months after starting chemotherapy (41.7 +/- 21.0 days) in the control group. The negativity of tuberculin skin testing was higher in the leukopenia group [7/14 (50%)] than in the control group [1/10 (10%)], however, the difference was statistically not significant due to rather small size of cases. Before the starting chemotherapy, the counts of WBC (7,230 +/- 1,530 vs 5,500 +/- 1,510/mm3, p < 0.001), neutrophil (5,230 +/- 1,450 vs 4,320 +/- 1,620/mm3, p < 0.05), lymphocyte (1,440 +/- 830 vs 830 +/- 440/mm3, p < 0.001) and platelet (34.9 +/- 12.2 vs 24.1 +/- 6.4 x 10(4)/mm3, p < 0.001) in the peripheral blood and the globulin level (3.71 +/- 0.61 vs 3.35 +/- 0.61 g/dl, p < 0.05) in the serum were significantly higher in the control group than in the leukopenia group. The decrements in the counts of WBC and granulocyte during chemotherapy were larger in the leukopenia group than in the control group (delta WBC: 2,880 +/- 1,530 vs 1,910 +/- 1,520/mm3, and delta Neut: 2,840 +/- 1,510 vs 1,820 +/- 1,380/mm3, p = 0.01, respectively), but the counts of lymphocyte were similar in both groups. The platelet counts also decreased in both groups, but to the mid-normal level in the control group, and to the lowest normal level in the leukopenia group, in which 15 out of 34 patients (44%) showed thrombocytopenia. The levels in the serum of hepatic enzymes such as AST, ALT, and gamma-GTP (gamma-glutamyl aminotransferase) increased during chemotherapy in the leukopenia group, while decreased in the control group, and the facts indicate that in the former not only bone marrow cells but also hepatic cells were impaired by anti-tuberculosis drugs. CONSIDERATIONS: Leukopenia may occur in the course of treatment with anti-tuberculosis drugs, but it is not necessary to stop the chemotherapy immediately, because the WBC count recovers spontaneously or remains under stable leukopenic state during chemotherapy in most cases. But when leukopenia appears, the peripheral blood counts must be checked cautiously, and the chemotherapy should be stopped if the WBC count progressively decreases. The patients who showed leukopenia due to anti-tuberculosis drugs may have had weaker natural and acquired (cell-mediated) immunologic response to tuberculosis infection, and more vulnerable bone marrow cells and hepatic cells to anti-tuberculosis drugs than the control.
Adult↗
The role of leukopenia in the 6-mercaptopurine-induced remission of refractory Crohn's disease.
OBJECTIVES: 1) to determine the frequency of induced leukopenia in patients with refractory Crohn's disease treated with 6-Mercaptopurine (6-MP). 2) to determine the influence of 6-MP-induced leukopenia on achieving remission [including the three major specific goals of therapy: (a) elimination or reduction of steroids, (b) healing of abscesses and fistulas, and (c) elimination of recurrent intestinal obstruction] and the effect on the rate and percentage of improvement in the CCFA-IOIBD index of Crohn's disease activity after 3 months of 6-MP therapy. 3) to determine whether an improvement of leukopenia was accomplished by an increased risk of clinical bone marrow depression. METHODS: We reviewed the course of 98 consecutive patients with refractory Crohn's disease treated with 6-MP and compared the 51 who developed leukopenia and the 47 who did not, in regard to achievement of remission, length of time until remission, rate of recurrence, and time until recurrence. RESULTS: 1) The mean time to remission was 8.8 wk for patients with leukopenia versus 14.3 wk for those without leukopenia. 2) A strong positive correlation exists between 6-MP induced leukopenia and the achievement and maintenance of remission in refractory Crohn's disease. This was evident in the analysis of response in specific goals and in the activity index. 3) There was no clinical evidence of bone marrow suppression in the 51 patients who developed 6-MP induced leukopenia. CONCLUSIONS: 1) Increasing the dose of 6-MP in patients with refractory Crohn's disease who have not yet responded and who have not achieved leukopenia will very likely increase the efficacy of this drug. 2) Influenced by the results of this study, we have launched a double-blind prospective study to evaluate the relationship between the induction of leukopenia with 6-MP and the achievement of remission.
Adult↗
Surgical resection deteriorates gemcitabine-induced leukopenia in pancreatic cancer.
BACKGROUND: Gemcitabine hydrochloride (GEM) is one of the most effective chemotherapeutic agents for pancreatic cancer; however, factors affecting GEM-induced leukopenia have not been clarified yet. In the present study, we analyzed the relationship between patients backgrounds and GEM-induced leukopenia. METHODS: Thirty-eight patients with pancreatic cancer were analyzed for correlation between the dose of GEM and the blood leukocyte number. Moreover, we compared leukopenia in resected and non-resected patients. RESULTS: The incidence of grade 3 or 4 leukopenia was 25% in the non-resected patients, whereas equivalent leukopenia was observed in 57% of the resected patients ( P = 0.048 by the chi(2) test). The relative decrease in blood leukocytes induced by GEM administration was more severe in resected patients (41.3 +/- 9.9%), as compared to non-resected patients (52.6 +/- 16.0%; P = 0.023 by t-test). CONCLUSION: In the present study, we found that the administration of GEM to patients after surgical resection caused more severe leukopenia, as compared to findings in non-resected patients. These data suggested that more frequent monitoring of the leukocyte count and prolonged intervals between GEM administrations are necessary for resected patients with pancreatic cancer.Gemcitabine hydrochloride (GEM) is one of the most effective chemotherapeutic agents for pancreatic cancer; however, factors affecting GEM-induced leukopenia have not been clarified yet. In the present study, we analyzed the relationship between patients' backgrounds and GEM-induced leukopenia.
Aged↗
Beta-Lactam antibiotic-induced leukopenia in severe hepatic dysfunction: risk factors and implications for dosing in patients with liver disease.
PURPOSE: To determine if an association could be established for leukopenia and administration of beta-lactam antibiotic therapy in patients with hepatic dysfunction. If such an association could be found, to determine the incidence, timing, and risk factors for beta-lactam antibiotic-induced leukopenia. PATIENTS AND METHODS: Patients with hepatic dysfunction, i.e., liver transplant recipients as well as patients with end-stage liver disease awaiting liver transplantation, seen at our institution between October 1989 and October 1991, who received 7 or more days of antibiotics, were studied in a prospective observational fashion. Complete blood count was determined at baseline and followed until the completion of the antibiotic course or until the resolution of leukopenia in leukopenic patients. RESULTS: Leukopenia occurred after a mean of 6 days with 23% of the beta-lactam antibiotic courses as compared with 0% with the non-beta-lactam antibiotic courses (p = 0.046). Development of leukopenia correlated with the severity of liver disease. Patients developing leukopenia had worse synthetic hepatic function as evidenced by a lower serum albumin level (p < 0.01), a lower serum cholesterol level (p < 0.05), and a higher prothrombin time (p < 0.01) as compared with the patients without leukopenia. Leukopenic patients had a lower baseline white blood cell count (p < 0.051) and a lower baseline platelet count (p < 0.01) indicative of a greater degree of hypersplenism. Leukopenic patients received a higher mean daily dosage of cephalosporins as compared with nonleukopenic patients. CONCLUSION: beta-Lactam antibiotics when administered in usually recommended dosages can induce leukopenia in patients with hepatic dysfunction. The probable mechanism is impaired hepatic metabolism of the beta-lactam antibiotics resulting in bone marrow suppression of white cell precursors from excessive antibiotic concentrations. The more severe the hepatic dysfunction, the greater the risk. We propose a reduction in dosages of beta-lactam antibiotics when used in patients with hepatic dysfunction. Finally, we raise the possibility that this adverse drug effect is more common than currently recognized by physicians.
Adult↗
Does chemotherapy-induced leukopenia predict a response in small-cell lung cancer?
The correlation between chemotherapy-induced toxicity and treatment outcome in cancer patients has not been studied thoroughly. Our aim was to evaluate whether there is any relationship between chemotherapy-induced leukopenia and response to treatment in small-cell lung cancer (SCLC). Data derived from records of 228 patients treated within two prospective multicentre phase II studies were analysed. In the first study (101 patients) chemotherapy included vincristine, epirubicin and cyclophosphamide and, in the second (127 patients), cyclophosphamide, etoposide and epirubicin; both regimens were given every 3 weeks. In the present analysis, the correlation between treatment outcome (response rate and survival) and highest scores of leukopenia within the first two and up to the fourth chemotherapy cycle, respectively, was evaluated. The objective response rate for the entire group was 66%; 53% in patients whose white blood cells remained normal and 85% in those who developed leukopenia within the first two cycles (P = 0.000). In multifactorial analysis, also including other treatment- and patient-related factors, independent correlation with response to chemotherapy was found for leukopenia (P = 0.001), chemotherapy regimen (P = 0.002) and the combined relative dose intensity (P = 0.018), but not for patient sex, age, performance status, pre-study weight loss, extent of disease and initial white blood cell count. Leukopenia within the first two cycles of chemotherapy was not correlated with survival, whereas such correlation for leukopenia occurring up to the fourth cycle was at the borderline level (P = 0.06). These findings suggest a relationship between chemotherapy-induced leukopenia and tumour response in SCLC.
Adult↗
Dialysis leukopenia, hypoxemia, and anaphylatoxin formation: effect of membrane, bath, and citrate anticoagulation.
The goal of these prospective studies was to determine the effect of different dialyzer membranes and dialysate composition on leukopenia and hypoxemia during hemodialysis with citrate anticoagulation. Significant early leukopenia was found with a cuprophane membrane, while a cellulose acetate membrane was associated with mild early leukopenia. Bath composition had no effect. Bicarbonate dialysate, compared with acetate, eliminated hypoxemia in cellulose acetate membranes and reduced its degree and duration with cuprophane. Membrane composition had no effect on hypoxemia during acetate dialysis. The findings indicate that leukopenia is directly and exclusively related to membrane composition while hypoxemia only relates in part to membrane effects. Serial determinations of complement components C3a and C5a showed significant increases in parallel with leukopenia during heparin anticoagulation, but the anaphylatoxin concentration changes were dissociated during dialysis with citrate anticoagulation. The concentrations of anaphylatoxins C3a and C5a appear not to be directly related to dialysis-induced leukopenia. The dissociation between anaphylatoxin concentrations and leukopenia may be related to changes in generation or unmasked changes in leukocyte response. Citrate anticoagulation may provide a useful probe for further studies on membrane-leukocyte interactions in vivo.
Acetates↗
Indirect-response model for the time course of leukopenia with anticancer drugs.
BACKGROUND: Because both the nadir count and the duration of leukopenia after chemotherapy with anticancer drugs are important, a pharmacodynamic model describing the entire time course of leukopenia is valuable. In this study, a pharmacodynamic model was developed to simulate leukopenia. METHODS: The model was developed with the 3-hour infusion data of paclitaxel. A concentration-time curve of paclitaxel for each patient estimated by a 3-compartment pharmacokinetic model was used as input to the model, which had 2 compartments corresponding to leukocytes in bone marrow and peripheral blood, respectively. Differentiation stages of myeloid cells sensitive to anticancer drugs were assumed, and exposure to a drug during their sensitive period as a function of time was used to inhibit the production of leukocytes in bone marrow. The model was validated by fitting the data of 24-hour infusion of paclitaxel or 14-day infusion of etoposide. RESULTS: Successful fitting of the leukopenia after a 3-hour infusion of paclitaxel was achieved. The following parameters were estimated: lag-time, 58 +/- 38 (mean +/- SD) hours before the leukocyte count started to decline; exposure giving 50% inhibition of leukocyte production (IC), 12.1 +/- 6.1 microg x h/mL; and sensitive period, 288 +/- 64 hours. These estimations were within physiologic ranges. In validation, leukopenia after 24-hour infusion of paclitaxel or 14-day infusion of etoposide was also explained by the model. Age was significantly negatively correlated with IC of paclitaxel (P = .039). CONCLUSIONS: This mechanistic model describes the time course of leukopenia and may provide a platform for pharmacodynamic analysis of anticancer drugs.
Adult↗
Role of peptidoglycan from Staphylococcus aureus in leukopenia, thrombocytopenia, and complement activation associated with bacteremia.
The role of the major cell wall components of Staphylococcus aureus in the leukopenia, thrombocytopenia, and complement activation associated with S. aureus bacteremia was studied in a guinea pig model. Formalin-killed S. aureus strains HSmR, 52A5, Cowan I, and Cowan EMS and purified peptidoglycan were used. Normal animals given peptidoglycan developed early (5-min) leukopenia, thrombocytopenia, and depletion of C3-C9 hemolytic activity similar to values in animals given killed S. aureus organisms and C4-deficient animals challenged with peptidoglycan. Cobra venom factor-treated animals challenged with peptidoglycan did not develop early leukopenia and thrombocytopenia, but all animal groups persistently had late (greater than 1-hr) leukopenia and thrombocytopenia. This observation suggests that peptidoglycan may play a major role in the early leukopenia and thrombocytopenia associated with S. aureus bacteremia in the guinea pig and that these effects can be mediated by activation of the alternative complement pathway alone. Peptidoglycan also causes a late leukopenia and thrombocytopenia which may occur independently of complement activation.
Animals↗
Pharmacodynamic modeling of the entire time course of leukopenia after a 3-hour infusion of paclitaxel.
The entire time course of leukopenia after anticancer treatment is clinically more relevant than a singly measured nadir count. In order to identify factors associated with neutropenic fever, a mechanistic pharmacodynamic model with two compartments corresponding to leukocytes in bone marrow and peripheral blood was applied to describe the time course of leukopenia. Seventeen patients with breast cancer were treated with 210 mg / m(2) of paclitaxel infused over 3 h as a single agent in a phase II study. Adequate fitting of the time course of leukopenia was achieved in all patients, and time-dependent parameters, including the time period during which leukocyte counts remained below 2000 / microl and the area between the curve for time versus leukocyte counts and the line of a leukocyte count of 2000 / microl (A < 2000), were calculated in each patient. Leukopenia was not significantly correlated with pharmacokinetic parameters, including time above a threshold concentration or the area under the time-concentration curve. A negative correlation between age and the sensitivity parameter of the pharmacodynamic model was observed (r (2) = 0.21, P = 0.07). Patients who experienced neutropenic fever had a larger A < 2000 than patients who did not experience fever (4512 vs. 6 days / microl, P = 0.05), but fever was not significantly related to any pharmacokinetic parameter or the leukocyte nadir count. Febrile episodes were better associated with the time course of leukopenia than the singly measured nadir count, and the pharmacodynamic model presents a novel platform to analyze the entire time course of leukopenia.
Adult↗
Deterioration of oxygenation and abnormal lung microvascular permeability during resolution of leukopenia in patients with diffuse lung injury.
To determine whether circulating leukocytes contribute to gas exchange abnormalities in diffuse lung injury, we retrospectively examined oxygenation in 6 patients who met 3 criteria: leukopenia caused by marrow aplasia from remission-inducing chemotherapy for myelogenous leukemia, the eventual resolution of leukopenia, and concurrent acute respiratory failure diagnosed clinically as increased permeability pulmonary edema. Four of the 6 patients abruptly developed overt clinical evidence of pulmonary dysfunction within the 96 h preceding the resolution of the peripheral leukopenia. In all 6 patients, the alveolar to arterial oxygen tension difference increased between leukocyte counts. The mean value for the alveolar to arterial oxygen tension difference for the group doubled during this period (148 +/- 37 mmHg 3 days prior to resolution; 290 +/- 37 mmHg 1 day after resolution; p less than 0.05). As an index of lung capillary permeability, we measured the lung permeability-surface area product for urea (PSu) for an additional patient with oxygen toxicity and drug-induced leukopenia whose hypoxemia increased immediately before the resolution of leukopenia. The PSu in this patient was high, in the range previously reported as being highly specific for increased permeability pulmonary edema with a fatal outcome. We conclude that such diffuse lung injury resembling the adult respiratory distress syndrome can occur in leukopenic patients, but the resolution of leukopenia in such patients may be associated with worsening oxygenation and with abnormally high pulmonary microvascular permeability. These observations do not prove a causal relationship but provide a clinical parallel to several leukocyte-depletion studies reported in animal models of increased permeability pulmonary edema that implicate white blood cells in the pathogenesis of hypoxemia and lung edema.
Adult↗
Alcoholism, leukopenia, and pneumococcal sepsis.
Pneumococcal bacteremia is associated with a high morbidity and mortality, especially when leukopenia is present. To define further the possible factors associated with death in pneumococcal bacteremia, we reviewed all cases at 2 hospitals over a 1-yr period. Overall, increased mortality was associated with women (p = 0.009), nosocomial acquisition of the disease (p = 0.001), the presence of leukopenia (p = 0.00002) or thrombocytopenia (p = 0.025), shock (p = 4 X 10(-8)), and adult respiratory distress syndrome (p = 2 X 10(-7)). Leukopenic and nonleukopenic patients were compared further to ascertain factors that may predispose to leukopenia. Alcoholism was the only associated condition correlating with the presence of leukopenia (p = 0.036), and alcoholism and leukopenia occurred in a group of younger men. We conclude that the association of alcoholism, leukopenia, and pneumococcal sepsis is a distinct clinical entity seen in younger patients and is associated with a very high mortality.
Alcoholism↗
Trovafloxacin-associated leukopenia.
OBJECTIVE: To report a case of trovafloxacin-associated leukopenia, which occurred in a trauma patient shortly after administration and resolved following discontinuation of the drug. CASE SUMMARY: A 79-year-old white man was admitted to Yale New Haven Hospital after sustaining partial amputation of his right lower leg by an industrial lawn mower. After successful resuscitation, he underwent complete right lower amputation and was treated with intravenous alatrofloxacin mesylate. He developed leukopenia that resolved after discontinuation of the drug. DISCUSSION: Trovafloxacin is a broad-spectrum synthetic fluoroquinolone used for a wide variety of bacterial infections. We report, for the first time in the English-language literature, a case of trovafloxacin-associated leukopenia. The leukopenia resolved promptly after discontinuation of the drug. This association is further supported by the exclusion of other potential causes for this adverse effect. CONCLUSIONS: Leukopenia is a well-recognized adverse effect of several drugs. We report a case of trovafloxacin-associated leukopenia during treatment of a trauma patient. Healthcare personnel should be aware of this possible adverse reaction in patients treated with trovafloxacin.
Aged↗
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↗
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↗