Disease relevance of Leukopenia

• Subsequently, manifestations of SLE develop, including leukopenia, proteinuria, and immune complex deposits in the kidney [1].
• A patient had cutaneous vasculitis, leukopenia, and splenomegaly caused by the antithyroid drug, propylthiouracil [2].
• Ibuprofen given at the mid-point of the infusion reversed the changes in all hemodynamic parameters, but had no effect on the leukopenia or thrombocytopenia [3].
• Because of the clinical toxicities associated with chronic Urd administration, the ability of benzylacyclouridine (BAU) to effect, in vivo, AZT-induced anemia and leukopenia was assessed [4].
• In contrast, the combined administration of PAF and endotoxin markedly elevated serum TNF alpha (1,359 +/- 362 pg/ml, n = 5, p less than 0.01) and thromboxane B2 (43 +/- 5 pg/100 microliters, n = 8, p less than 0.01) along with hypotension, hemoconcentration, leukopenia, and thrombocytopenia [5].

Psychiatry related information on Leukopenia

• Similarly to the 16/6 Id-immunized mice, the mice injected with the anti-16/6 Id mAb exhibited elevated erythrocyte sedimentation rate and leukopenia [6].
• Azathioprine-induced leukopenia was uncommon (19 episodes in the triple therapy group) [7].

High impact information on Leukopenia

• Crossovers from trimethoprim-sulfamethoxazole to aerosolized pentamidine were more common than the reverse (27 vs. 4 percent), partly because of the study protocols for the management of leukopenia [8].
• Successful treatment required resolution of aplasia or leukopenia, catheter removal, systemic treatment with amphotericin B, and local wound care [9].
• The use of lithium carbonate to reduce infection and leukopenia during systemic chemotherapy [10].
• Pediatric ibuprofen and leukopenia [11].
• The other 631 ADEs were detected from automated signals, the most common of which were diphenhydramine hydrochloride and naloxone hydrochloride use, high serum drug levels, leukopenia, and the use of phytonadione and antidiarrheals [12].

Chemical compound and disease context of Leukopenia

• Leukopenia secondary to sulfadiazine silver [13].
• Two other patients were found to have leukopenia after initial therapy with sulfisoxazole [14].
• Leukopenia following treatment with thiothixene and haloperidol [15].
• Forty-five percent of the patients receiving bolus 5-FU alone (A) experienced grade 3-4 leukopenia, with two sepsis-related deaths [16].
• In contrast, neither antibody titer was significantly associated (P less than or equal to 0.05) with patients' age or sex, severity of underlying disease, presence of leukopenia, steroid or immunosuppressive therapy [17].

Biological context of Leukopenia

• RESULTS: Regression analysis showed that carboplatin AUC, prior treatment, and Eastern Cooperative Oncology Group grade performance status (PS) are predictors of tumor response, thrombocytopenia, and leukopenia [18].
• 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 [19].
• The supplemental vitamin A prevented the impaired wound healing and lessened the weight loss, leukopenia, thrombocytopenia, thymic involution, adrenal enlargement, decrease in splenic weight, and gastric ulceration of the radiated (750-850 rad) wounded rats [20].
• Complement activation, as judged by venous plasma C3a levels, was also temporally correlated with hemodialysis leukopenia [21].
• These changes correlated with the toxic effect of cyclophosphamide on the wall of the bladder rather than with peripheral leukopenia or failure of antibody response [22].

Anatomical context of Leukopenia

• To determine whether invading leukocytes mediate these responses, acute inflammatory cell influx was suppressed either by inducing leukopenia with nitrogen mustard or by administration of BW-755C, a mixed cyclooxygenase-lipoxygenase inhibitor [23].
• We have engineered transgenic mice that express this multidrug transporter in their bone marrow and demonstrated that these animals are resistant to leukopenia by a panel of anticancer drugs including anthracyclines, vinca alkaloids, etoposide, taxol, and actinomycin D [24].
• LPS-induced pulmonary vascular injury was significantly attenuated in rats with nitrogen mustard-induced leukocytopenia and in rats treated with ONO-5046, a potent granulocyte elastase inhibitor [25].
• The induction of leukocytopenia had the same effect as APC, in that it significantly reduced motor disturbances, tissue levels of TNF-alpha, and neutrophil accumulation in the animals subjected to compressive SCI [26].
• Potential risk factors included RA severity measures (rheumatoid factor positivity, elevated erythrocyte sedimentation rate, extraarticular manifestations of RA, and functional status), comorbidities (diabetes mellitus, alcoholism, and chronic lung disease), and other risk factors for infection (presence of leukopenia, smoking) [27].

Gene context of Leukopenia

• Furthermore, severe leukopenia was abrogated in all the cycles supported with IL-3+G-CSF, while in the cycles without cytokines, this event was registered in 62.5% of the cases (p < 0.0005) [28].
• We found the frequency of leukopenia episodes (WBC < 4.0 x 10(9)/L) significantly higher in heterozygous patients (53.8%) compared with those with TPMT wild-type genotype (23.5%) [29].
• The most efficient diagnostic approach is to assume erythropoietin deficiency, exclude iron deficiency, and pursue further diagnostic tests only when red-cell indices are abnormal or when leukopenia or thrombocytopenia are also present [30].
• To ascertain the consequences of severe leukopenia and the tempo of recovery, we studied the immunity of 56 adult patients treated for multiple sclerosis or systemic sclerosis with autologous CD34 cell transplantation using extremely lymphoablative conditioning [31].
• During leukopenia (<10(9) cells/liter), LPS stimulation of whole blood did not result in an increase in IL-8 levels [32].

Analytical, diagnostic and therapeutic context of Leukopenia

• CONCLUSIONS: This dose-intensive regimen can be given safely without progenitor replacement. rhu GM-CSF decreases the duration of severe leukopenia and decreases the need for hospitalization and antibiotic therapy [33].
• Hemodialysis of 11 endstage renal failure patients with new cuprophan hollow fiber dialyzers produced significant leukopenia as well as increased plasma levels of both C3a and C5a antigens during the initial phases of the procedure [34].
• CONCLUSIONS: NM conditioning with posttransplant immunosuppression using CsA and MMF resulted in less leukopenia and fewer transfusions, but resulted in more cases of graft failure, acute GVHD, and TRM than in RIC patients [35].
• BACKGROUND: Our study assessed the factors that predispose renal transplant recipients to the occurrence of thrombocytopenia and leukopenia, as well as the severity and the time- and concentration-dependence of these side-effects, after administration of sirolimus (SRL) in combination with a cyclosporine (CsA) and prednisone (Pred) regimen [36].
• The polysaccharide showed no indications of toxicity in mice at doses far in excess of the lethal dose for the parent glycolipoprotein, nor did the mice develop the leukopenia that characteristically follows intraperitoneal injection of glycolipoprotein [37].

References