Rise In Leukocyte Count Research Articles

Unraveling florfenicol's effects on splenic histology, erythrocytes, and hematology of healthy Oreochromis niloticus juveniles

AbstractThe study aimed to investigate the impact of administering the antibiotic florfenicol (FFC) through dietary means on Oreochromis niloticus. The experiment involved exposing the fish to FFC at doses 0–10 times the therapeutic dose of 15 mg/kg biomass per day for 10 consecutive days. The group receiving the therapeutic dose showed 100% survival on the 10th day of dosing. Histological analysis revealed dose‐dependent changes in the spleen, including an increase in sinusoidal space, splenic necrosis, white pulp proliferation, splenitis, and red pulp hemorrhages. Additionally, there was an exponential rise in leukocyte counts accompanied by a significant decrease in erythrocyte counts, indicating the development of anemia due to FFC. The observed splenic histological damage, along with increased erythrophagia, erythro‐membrane breakage, and poikilocytosis, highlighted the splenotoxic and hemotoxic effects of FFC at higher doses. Importantly, these toxic effects showed considerable reduction upon discontinuation of FFC dosing. The study emphasized the need to consider FFC‐induced splenotoxic and hemotoxic outcomes in O. niloticus during its application in aquaculture.

Combination of
 omega-3 polyunsaturated fatty acids and statins for the prevention of atrial fibrillation after coronary bypass surgery

Aim. To evaluate the influence of combination of omega-3 polyunsaturated fatty acids and atorvastatin on the risk of atrial fibrillation (AF) after coronary bypass surgery (CBS). Material and methods. The study included 114 patients divided into 2 groups, one comprised of 59 ones (75,6% men of mean age 62,0±7,3 yr given conventional medication), the other including 55 patients (80,0% men of mean age 59,4±6,7 yr given omega-3 polyunsaturated fatty acids 5 days before (2 g/d) and during 3 weeks after CBS (1 g/d)). All patients were treated with atorvastatin at the outpatient stage. IL-6,8, 10 and C-reactive protein (CRP), fibrinogen, troponin, NT-proBNP, superoxide dismutase (SOD), and myeloperoxidase were measured at admittance and on day 3.7±1.4 after surgery. Results. AF developed on day 5.9±4.9 (mean) after surgery. Patients of group 2 tended to have fewer new episodes of arrhythmia although no significant difference between the groups was documented (9,1% vs 18,6%, р=0,12). Group 2 included more smokers (74,5% vs 45,8%, р=0,002) and patients with atherosclerosis of lower limb arteries (87,3% vs 71,2%, р=0,03) but fewer those consuming nitrates (39,0% vs 18,2%, р=0,01) and Ca antagonists (45,8% vs 21,8%, р=0,006).Mean dose of atorvastatin given to patients of groups 1 and 2 was 24.7±12.5 and 25.1±10.5 mg/d respectively (р=0,2), duration of its intake 14.6±12.7 and 21.5±19.3 months (р<0,001). There. was no significant difference between leukocyte count, leukogram, IL-8, IL-10, NT-proBNP, and troponin levels before and after CBS. Surgical myocardial revascularization caused a rise in leukocyte count, shifted the leukogram toward predominance of stab and segmented cells, increased IL-8, IL-10, fibrinogen, NT-proBNP, CRP, and troponin levels in both groups. IL-8 and IL-10 levels remained normal before and after surgery. Preoperative IL-6 level in group 1 was significantly higher than in group 2 (21,7±13,0 vs 2.5±2,2 pg/ml, р<0,001). Postoperatively, the difference was absent. The CRP level before surgery was high in both groups (3122.7±2175.8 vs 3670.8±2490.0 U/g) but decreased after CBS although remained higher in group 1 (1957.6±1660.3 vs 1069.8±630.2 U/g, р<0,001). Myeloperoxidase level increased postoperatively in both groups but the difference was insignificant. Fibrinogen and CRP in the postoperative period increased more significantly in group 2 than in group 1 (4,9±1,4 vs 4,4±1,1 g/l, р=0,02 and 8,6±2,2 vs 5,4±2,3 mg/l respectively, р<0,001). Conclusion. The study revealed an insignificant decrease in the number of AF episodes in the early post-CDS period in patients treated with omega-3 polyunsaturated fatty acids and atorvastatin compared with those given the latter medication alone. Also, fibrinogen and CRP levels as markers of inflammation increased while SOD antioxidative activity decreased.

The enlarged spleen – a blood bank

Splenomegaly may be the result of several diseases such as myeloproliferative disorders, portal hypertension etc. Sometimes the splenic size may assume massive proportions. A massive splenomegaly may lead to symptoms or changes in laboratory parameters over and above the original disease state. The predominant symptoms include pain due to the splenic infarcts, dragging sensation due to the sheer size, early satiety etc. It has been known for several decades that a large spleen is a massive pool of sequestered blood cells. It can be holding 30–90% of all platelets and 40% of all erythrocytes. The bone marrow is typically hypercellular to compensate for this sequestration. Splenectomy entails removal of the whole spleen along with the sequestered blood cells in the spleen. This seems like a terrible waste of the sequestered blood components. If one was able to harvest these components the potential benefits could include a rise in the hematocrit, possibly avoidance of blood transfusion, immediate rise in platelet count, with implications for hemostasis and a rise in leucocyte count. The potential secondary benefits may include easier handling of a smaller spleen, reduced blood loss and lesser operation time. While it is quite common practice to ligate the splenic artery first, during splenectomy for a massive splenomegaly, the objective benefits of this step have been studied by few. This step of the surgical procedure is commonly performed by surgeons to reduce the problems of handling a massive spleen and, possibly, reduce blood loss during peri-splenic dissection, particularly in patients with portal hypertension. The ‘auto-transfusion’ of sequestered components is but a side-effect of this step. One concern of such an auto-transfusion is the quality of blood cells being released into the blood stream. Other potential concerns are the risks of dissecting the large tortuous splenic artery, especially in patients with portal hypertension, in the face of unquantified benefits. The study by Madhavan et al in this issue of the journal studied the objective benefit of early ligation of the splenic artery during splenectomy for portal hypertension.They studied 30 patients with portal hypertension (NCPF 20, EHPVO 9, Cirrhosis 1) who underwent splenectomy and proximal spleno-renal shunt in their unit. They found that there is significant increase in the RBC and platelet counts, though there was no statistically significant increase in the total leucocyte count, differential leucocyte count and hemoglobin. Even though the study suffers from several methodologic flaws it does bring into focus the auto-transfusion benefits of early ligation of the splenic artery during splenectomy. However the study does not report the percentage changes in the cell counts and only the mean values have been used for analysis instead of paired analysis. Gazula et al had earlier studied a similar population and reported a significant increase in the hemoglobin, hematocrit, leucocyte, platelet and RBC counts after early ligation of the splenic artery. They had restricted intravenous fluid administration after splenic artery ligation and thus found that benefits extended to increased hemoglobin, hematocrit and leucocyte count also. Both the studies excluded patients requiring intravenous fluids or blood transfusion and did not include a control population. While this may have removed the confounding

LABORATORY TESTS IN PATIENTS WITH ACUTE APPENDICITIS

Laboratory measurements such as leucocyte count, neutrophil percentage and C-reactive protein (CRP) concentration are commonly used as diagnostic aids in patients with suspected acute appendicitis. The present study aimed to clarify the role of these laboratory tests in diagnosing acute appendicitis. The medical records of 897 patients who underwent appendicectomy for suspected acute appendicitis during a 30-month period were retrospectively reviewed. The laboratory findings were correlated with the histopathology of the excised appendices. Data were analysed to calculate the sensitivity and specificity of the individual tests, as well as the test combinations. Histologically verified appendicitis was found in 740 of the 897 patients (82.5%). The rise in leucocyte count and neutrophil percentage correlated with the degree of appendiceal inflammation. The median CRP level was much higher in the patients with ruptured appendicitis compared with that in patients with a normal appendix (96.8 vs 39.6 mg/L, P < 0.001). However, patients with uncomplicated appendicitis had a lower median CRP concentration than those with a normal appendix, although the difference was not statistically significant (24.1 vs 39.6 mg/L, P = 0.079). The sensitivity of leucocyte count, neutrophil percentage and CRP in diagnosing acute appendicitis was 85.8, 87.2 and 76.5%, respectively, whereas the specificity was 31.9, 33.1 and 26.1%, respectively. Of the 740 patients with acute appendicitis, only six had all three tests simultaneously within the reference interval. Abnormal laboratory findings cannot reliably deliver a diagnosis of acute appendicitis. However, acute appendicitis is very unlikely when leucocyte count, neutrophil percentage and CRP level are simultaneously normal.

Severe hypophosphatemia during hematopoietic reconstitution after allogeneic peripheral blood stem cell transplantation

A patient suffering from acute myeloid leukemia (FAB M5a) received a PBSC allograft from a matched, related donor. On day 13 after transplantation severe hypophosphatemia (0.21 mmol/l) was first noted which persisted irrespective of intravenous phosphate administration, and within 2 days reached concentrations below 0.13 mmol/l. After repeated phosphate substitution serum phosphate returned to 1.40 mmol/l on day 17. Phosphate in urine, and calcium in serum were recorded as unchanged throughout. Clinical signs and symptoms due to severe hypophosphatemia were not observed except for paresthesia in the lower extremities. The precipitous fall in serum phosphate coincided with hematopoietic reconstitution as reflected by a steep rise in leukocyte count from 0.08 x 109/l on day 10 to 5. 94 x 109/l on day 15 after transplantation. Thus, isolated hypophosphatemia was likely the result of excessive cellular phosphate uptake during hematopoietic reconstitution. Electrolyte monitoring after PBSCT should include serum phosphate to identify the hypophosphatemia associated with hematopoietic recovery.

The influence of acute smoking on leucocytes, platelets and the endothelium

Cigarette smoking is a risk factor for the development of atherosclerosis. Possible mechanisms for this include leucocytes and platelet activation, and/or damage to the endothelium, any of which may contribute to changes in thrombosis and haemostasis. We examined the acute effects of smoking on these systems by obtaining blood before, immediately after, and at 10 and 30 min after the rapid smoking of two cigarettes in sequence by 20 smokers. Blood samples taken at the same time points from ten non-smokers acted as control material. In the smokers there was a transient rise in leucocyte count and neutrophil activation, but von Willebrand factor (VWF—marking endothelial damage) increased steadily at each time point ( P<0.05). There were no changes in neutrophil elastase, soluble intercellular adhesion molecule-1 (sICAM-1—normally increased in smokers), fibrinogen, platelet count or soluble P-selectin (marking platelet activation, also normally increased in smokers). We conclude that the acute smoking of two cigarettes in succession will activate leucocytes and cause endothelial cell damage, but will not immediately influence platelet activity.

Early Mortality and the Retinoic Acid Syndrome in Acute Promyelocytic Leukemia: Impact of Leukocytosis, Low-Dose Chemotherapy, PMN/RAR-α Isoform, and CD13 Expression in Patients Treated With All-Trans Retinoic Acid

All-trans retinoic acid (RA) has proven a major advance in the treatment of acute promyelocytic leukemia (APL). However, the proper management of patients who present with or develop leukocytosis during remission induction with all-trans RA is not established, nor is there a clear relation between leukocytosis and the development of the retinoic acid syndrome. We reviewed the course of our patients who underwent induction with all-trans RA to identify potential factors that might predict for the development of this syndrome and to identify which patients, if any, might specifically benefit from additional treatment with cytotoxic chemotherapy. Seventy-eight courses of all-trans RA therapy were administered to patients with a molecular diagnosis of APL. Initial and peak leukocyte counts, their rate of rise, leukocyte count criteria developed in Europe, and cell surface marker expression were all analyzed relative to subsequent development of both the RA syndrome as well as all causes of early mortality. The outcome of patients who received specific treatment for retinoid-induced leukocytosis was also examined. No factor was found to consistently predict for the development of the RA syndrome. Although the occurrence of the syndrome was positively associated with the peak value of the peripheral blood leukocyte count (P = .001), neither the initial leukocyte count nor the rate of rise in leukocyte counts on days preceding onset of the syndrome were sufficiently well-correlated to be clinically useful (P = .21). The leukocyte count criteria developed in Europe had a sensitivity of 62%, a specificity of 69%, and a positive predictive value that ranged from only 44% to 72%. However, we unexpectedly found that basal expression of CD13 (aminopeptidase N), a cell surface enzyme previously linked to tumor cell invasion and an inferior outcome in patients with acute myeloid leukemia, was highly associated with both development of the syndrome (P < .05) as well as an elevated leukocyte count (P = .006). Neither low-dose chemotherapy nor leukapheresis prevented development of the syndrome nor ameliorated its effects. In fact, 9 of 11 patients who received these interventions sustained fatal or near-fatal events, most of which were due to hemorrhage. However, early treatment with a short-course of high-dose corticosteroids halted progression of the syndrome in most cases. Finally, we found that expression of the type "A" isoform of PML/RAR-alpha (also known as bcr3 or "short") was associated with a significantly shorter duration of relapse-free and overall survival (P = .005).(ABSTRACT TRUNCATED AT 400 WORDS)

High-dose IgG for neutropenic patients with acquired immunodeficiency syndrome (AIDS)

Leukocytopenia and bacterial infections are common and serious complications in patients with AIDS. We report here on three patients in whom the administration of high IgG doses led to gradual (two patients) or prompt (one patient) increases in circulating leukocyte counts (from 200-600 to 2500-5900/microliters), inducing definite improvement in two patients; one patient died from Pneumocystis carinii pneumonia. Although the rise in leukocyte counts lasted for only approximately 3 weeks, high-dose IgG might be a useful therapeutic adjunct in such patients.

Repeated membrane plasma separation with on-line sorbent treatment of plasma in the conscious rat.

Repeated membrane plasma separation with on-line sorbent treatment of plasma was performed in unrestrained and conscious rats, thus avoiding the possible effects of repeated stress and exposure to anesthetic agents. The procedure was well tolerated, even after four consecutive perfusions. Blood flow was 0.7 ml/min, with a transmembrane pressure of 18.6 mm Hg and plasma filtration rate of 0.21 ml/min. This allowed 12 ml of plasma (greater than 1 plasma volume) to be treated within 1 h. Levels of albumin, immunoglobulin G, and C3 remained constant during each perfusion and were not significantly different from those of animals subjected to control procedures. Results obtained from filtrate were comparable at 15 and 60 min with values obtained from whole blood, with sieving coefficients of approximately 1. Leukocyte, erythrocyte, and thrombocyte counts remained unchanged during each plasma perfusion. A progressive rise in leukocyte counts occurred following successive perfusions, but this was true also of animals subjected to control procedures.

Study of factors determining the usefulness and complications of leukocyte transfusions

Fifty-two patients suffering from severe neutropenia were treated with leukocyte transfusions. Except for two of these patients, who received cells from normal donors, the cells transfused were obtained from patients with chronic myeloid leukaemia. In 50 per cent of the patients the transfusions were followed by disappearance of fever and associated signs of infection, and a rise in the leukocyte count, which was dependent on the establishment of a graft by the transfused cells. The rise in leukocyte count occurred when chronic myeloid leukaemia cells were transfused into the recipients. The beneficial symptomatic effects of the transfusions were obtained only when a sufficiently large number of cells was given. In twenty-four patients with acute leukaemia given these transfusions nine remissions were induced by this treatment. No anticancer effect was noted in diseases other than acute leukaemia. The antileukaemic effect is related to a graft versus host reaction. The reaction produced by the transfusions of cells was identical with the secondary syndrome that complicates the grafting of allogeneic bone marrow in man. The frequency of this syndrome did not depend on the underlying disease but, as with the antileukaemic effect in acute leukaemia, on the number of cells transfused. Incubation of the cells to be transfused for two hours at 37 °C. reduced the frequency and severity of the secondary syndrome without affecting their ability to produce a symptomatic effect. Storage of the transfused cells at −70 °C. reduced the severity and frequency of the secondary syndrome but also the value of these transfusions to combat the agranulocytosis syndrome.