Development Of Thrombocytosis Research Articles

Clinical and hematological сhanges in viral panleukopenia in cats

Cat infectious diseases have become widespread due to the increase in the number of stray cats; feline viral panleukopenia is no exception. It is caused by a single-stranded DNA virus of feline parvovirus, characterized by high contagiousness, fever, damage to the gastrointestinal tract, respiratory organs, heart, general intoxication, and body dehydration. The research aimed to study the hematological indices of blood and biochemical indices of plasma in viral panleukopenia of cats. During the development of intestinal panleukopenia syndrome in animals, vomiting and diarrhea were noted. The development of inflammatory processes in the digestive organs causes pain in the abdominal cavity, due to which a specific “sitting posture” occurs. An acute course was most frequently noted, characterized by a sudden increase in temperature to 42 °C, vomiting, diarrhea, and cachexia. Studies of hematological indices of blood indicate the development of thrombocytosis, neutrophilia, monocytosis, and lymphocytosis, which corresponds to the acute course of the disease with a focal inflammatory process. Erythropenia leads to systemic disorders of the cardiovascular system, which provoke the weakening of the body, accompanied by cachexia. Studies of biochemical parameters of plasma indicate systemic disorders of organs developing in the body. Thus, an increase in total protein indices and globulin fractions indicates inflammatory processes in the body, particularly the digestive and urinary organs. In addition, one of the renal impairment indices was an increase in creatinine and urea, and an increase in glucose, total bilirubin, AST, and α-amylase indicates liver and pancreas dysfunction. In some cases, hepatitis and infectious toxicosis may develop. The study of hematological indices of blood and biochemical indices of plasma will ensure a complex picture of morphological changes that develop in the body of cats with panleukopenia. The obtained data will permit the monitoring of an animal's condition with the applied therapeutic scheme and the form of a prognosis.

1146. Thrombocytosis in Infants with Congenital Cytomegalovirus Infection Being Treated with Valganciclovir

BackgroundCongenital CMV (cCMV) is associated with sensorineural hearing loss and neurodevelopmental disabilities. Infants with symptomatic cCMV infection benefit from 6 months of oral valganciclovir (vGCV) therapy. Neutropenia, thrombocytopenia, and hepatotoxicity are adverse effects vGCV, for which we monitor. We observed a pattern that cCMV infants treated with vGCV developed an uptrend in platelets and/or thrombocytosis (platelet count >450,000/uL) while on therapy. This observation has not previously been reported.MethodsMedical records and laboratory results from our multi-disciplinary cCMV clinic led by Infectious Diseases at Lurie Children’s Hospital were reviewed (2017-2020). Data included cCMV signs/symptoms, cCMV treatment prescribed, indication for ganciclovir/vGCV treatment, and complete blood count prior to, during, and post- vGCV therapy.ResultsOf 21 cCMV infants referred to clinic, 14 received >1 month of vGCV for symptomatic disease, 1 discontinued vGCV < 1 month due to perceived fussiness, and 1 was part of a clinical trial. Four infants were initially treated with ganciclovir for ≤1 month and transitioned to vGCV. Of the 14 patients treated with vGCV, 10 (71%) had sensorineural hearing loss (50% unilateral), 12 (86%) had central nervous system abnormalities (including cystic lesions on head ultrasound), 5 (36%) had thrombocytopenia, and 7 (50%) were intrauterine growth restricted [Table 1]. Eleven infants (79%) developed thrombocytosis. Thirteen infants (93%) had an uptrend in platelet count [not including normalization of initial thrombocytopenia (platelets < 150,000/uL)]. Figure 1 shows platelet counts by time with respect to vGCV treatment. Neutropenia (absolute neutrophil count < 500/uL) occurred in 1 patient that required temporary discontinuation of vGCV.Table 1 Figure 1 ConclusionWe observed an interesting trend of rising platelet count and the development of thrombocytosis in the majority of our cCMV patients on vGCV. Platelet elevation associated with vGCV has not previously been described. This observation is limited by small number of patients and thrombocytosis is not a definitive association/adverse effect. With increasing use of vGCV and interest in its effect on bone marrow function, this observation is notable and warrants further study.Disclosures All Authors: No reported disclosures

Is thrombocytosis always an indicator of autosplenectomy in patients with systemic lupus erythematosus?

In systemic lupus erythematosus (SLE), the most commonly encountered finding related to platelets is thrombocytopenia whereas thrombocytosis is rarely reported. Our aim here was to reveal the type and the frequency of thrombocytosis in SLE patients along with its causes. Data of patients were evaluated retrospectively. Patients who had a platelet count of > 450,000/mm3 (> 450 × 109/L) in at least two subsequent counts and lasting more than 6months during the follow-up were considered to have "persistent thrombocytosis". Peripheral smear results of patients with thrombocytosis were analyzed, and spleen imaging was performed for autosplenectomy/hyposplenism to patients with persistent thrombocytosis. A total of 205 patients with SLE were included in the study [196 (95.6%) female, mean age 41.5years]. Out of 12 patients (5.9%) with thrombocytosis, 9 (4.3%) had transient thrombocytosis and 3 patients (1.4%) had persistent thrombocytosis. Of those with transient thrombocytosis, 5 were associated with iron deficiency anemia (IDA), 2 to polyarthritis, and the remaining 2 to digital ischemia and/or cutaneous vasculitis. Of three patients with persistent thrombocytosis, one was identified to have had splenectomy due to resistant immune thrombocytopenic purpura, and the other two (0.9%) patients had autosplenectomy. The only independent risk factor for the development of thrombocytosis was the presence of cutaneous vasculitis (OR 10.79 (95% CI 2.14-54.47), p = 0.0004). During the course of SLE, frequency of thrombocytosis is similar to that of the general population and the most common cause is reactive thrombocytosis. If the thrombocytosis was persistent, rheumatologist must consider that the patient may have autosplenectomy/asplenia/hyposplenism.

325 Thrombocytosis as a Predictor of Outcome In Severe TBI

Abstract INTRODUCTION Post-traumatic development of thrombocytosis is felt to be secondary to a reactive process associated with cytokine release during the global inflammatory state and has been demonstrated in a general trauma population to be associated with decreased mortality. This has not been investigated in patients with severe traumatic brain injuries. METHODS This study included 120 consecutive patients with severe TBI (GCS&lt;8) presenting to our institution between 6/2010 and 9/2012. Clinical data was retrospectively collected; clinical outcomes were part of a prospective registry. Exclusion criteria included non-survival to hospital discharge and lack of follow up data. Thrombocytosis was defined as peak platelet count greater than 600 × 103/mm3. Primary outcome was Glascow Outcome Score at 6 months. Secondary outcome was mortality at 6 months. RESULTS &gt;Forty-four patients were available for analysis after applying exclusion criteria. All patients demonstrated an increase in platelet counts when compared to admission levels. Twenty-one (47%) patients developed thrombocytosis during their hospital stay with an average platelet count of 752 × 103/mm3 and an average time to peak of 17 days. Patients who developed thrombocytosis had a trend towards decreased GOS at 6 months (3.3 vs 3.8, p = .08) and towards longer hospital stays (37.5 vs 21.5, p = .08). Six-month mortality was unchanged between the two groups (4% vs 4%, P = 1). Additionally, patients with peak platelet counts that were greater than 200% of admission baseline had lower GOS at 6 months when compared to those that remained below 200% of baseline (3.4 vs 4.1, p = .03). CONCLUSION The development of post-traumatic thrombocytosis, while associated with lower mortality in the overall trauma population, may be associated with worse outcomes and longer hospital stays in patients with severe traumatic brain injuries. Relative reactive thrombocytosis greater than 200% of baseline may be more predictive of poor outcome than strictly defined laboratory cutoffs.

Etiology and clinical relevance of elevated platelet count in ICU patients : Aretrospective analysis.

Thrombocytosis is acommon phenomenon in critically ill patients. Although thrombocytosis is an independent risk factor for complications, it does not seem to influence mortality in intensive care (ICU) patients. Our investigation aimed to evaluate the etiological and clinical relevance of aplatelet count greater than 450× 109/l in ICU patients. Patients admitted for aminimum of 4days to an interdisciplinary ICU during a45-month period were enrolled in this retrospective observational study. Thrombocytopenic patients (platelet count <150× 109/l in at least one measurement) were excluded. The study patients were divided into two groups: thrombocytosis group (thrombocytes >450× 109/l in at least one measurement) and control group (thrombocytes= 150- 450× 109/l during ICU stay). Univariate and multiple regression analysis were used to determine the influence of severe co-morbidities on the development of thrombocytosis and the association of elevated platelet count with thrombotic embolism, length of stay (LOS) in ICU, and mortality. Atotal of 307 patients were analyzed, of whom thrombocytosis was observed in 119 cases. Independent risk factors for the development of thrombocytosis included SIRS, mechanical ventilation, and acute bleeding. Increasing age reduced the risk of thrombocytosis. Thromboembolism occurred in 16patients (13.4%) with an elevated platelet count and only in nine patients (4.7%) with physiological platelet values (OR: 3.1; 95% CI: 1.3-7.2; p= 0.009). Mean duration of LOS was significantly longer in patients with thrombocytosis (25.2 vs.11.7 days, p< 0.0001). Elevated platelet count showed anegative correlation with ICU mortality (OR: 0.32; 95%-CI: 0.12-0.83; p= 0.019). In our retrospective analysis the occurrence of thrombocytosis in acohort of interdisciplinary ICU patients was associated with a higher rate of complications and longer LOS in the ICU. Despite these findings, thrombocytosis seems to reduce mortality in critical ill patients.

Relationship of postoperative thrombocytosis and survival of patients with colorectal cancer

IntroductionThrombocytosis accompanying solid tumors and predicting the prognosis of malignant tumors has been the subject of intensive research lately. Reports so far have evaluated the role of preoperative platelet count. In our present study we looked at the effect of tumor removal on platelet count and the predictive power of postoperative thrombocytosis on the survival of patients with colorectal cancer (CRC). MethodsWe retrospectively evaluated the clinical and histopathological data of 336 patients operated due to CRC between 2001 and 2011. Thrombocytosis was defined as a platelet count exceeding 400 × 103/μL. Preoperative platelet count was compared with the value measured 1 month postoperatively. ResultsThe platelet count significantly decreased after the removal of the primary tumor (paired Wilcoxon test p < 0.001). In univariate analysis preoperative thrombocytosis was a significant marker of overall survival (OS) with HR 2.2, p < 0.001 while the postoperative thrombocytosis was nearly significant with HR = 1.59, p = 0.087. In multivariate setting, when corrected for location, stage, tumor size and controlling for gender and age (>65 years vs. ≤65 years), both pre- and postoperative thrombocytosis were significant independent prognostic markers with HR 1.80, p = 0.20 and HR = 1.98, p = 0.018, respectively. Discussion and conclusionAlthough the pathomechanism of thrombocytosis related to solid tumors is not known the decrease of platelet count after the removal of the primary tumor raises the possibility that the tumor may play an active role in the development of thrombocytosis. Furthermore, the observation of postoperative thrombocytosis with significant worse outcome underlines the predictive power of elevated platelet count.

Extreme thrombocytosis in a traumatic patient

Encountering abnormally high values of platelet in patients who do not have a clonal hematologic disease is a phenomenon known as secondary or reactive thrombocytosis, which is considered a normal response after inflammatory insults, such as infection, surgery, or trauma [1]. After trauma, development of thrombocytosis is common, as reported in the prior studies, in which about 20% of patients had a platelet count above 450,000/µl, and with respect of extreme thrombocytosis (platelet count above 1,000,000/µl), the incidence is approximately 1.4-5.7% in trauma patients [1,2]. The anesthesiologists have to consider whether this condition be managed with anticoagulants to prevent thromboembolic event. We report our experience of perioperative management of a patient with reactive thrombocytosis. An 83-year-old woman was scheduled for dynamic hip screw fixations for right intertrochanteric fracture. Her medical and surgical histories were uneventful. The baseline laboratory investigations revealed extreme thrombocytosis (platelet count 1,430,000/µl), borderline derangement in coagulation parameter (aPTT 46.4 sec, 1.20 INR) and marginal leukocytosis. Preoperative electrocardiogram and chest radiograph were unremarkable. Despite the marked thrombocytosis, physical examination revealed no evidence of arterial occlusive disease. We considered the thrombocytosis due to secondary cause - trauma; because the patient experienced trauma, there was no previous medical history, and the C-ractive protein was elevated. We recommended using anticoagulant in the perioperative period because the patient was an old woman with femur fracture, but anticoagulant was not used due to a fear of bleeding tendency. The patient underwent an operation under general anesthesia. The induction of anesthesia was performed with propofol and rocuronium. After a tracheal intubation, the left radial artery was cannulated. Anesthesia was maintained with sevoflurane in N2O/oxygen. There was no significant intraoperative event and the recovery from anesthesia was uneventful. During a perioperative period, we had closely observed the patient to observe whether the deep vein thrombosis or arterial occlusive events developed. There was no thromboembolic complication on the postoperative 9 months follow-up. The platelet count was gradually decresed and laboratory studies demonstrated an normal platelet count (434,000/µl) on the 39th postoperative day. So, should this condition be managed with anticoagulant to prevent thromboembolic or other events? If the extreme thrombocytosis is caused by reactive thrombocytosis, there is no evidence showing any benefit to anticoagulant therapy, and then a significantly higher incidence of wound infections was reported in patients who were treated with aspirin, compared with patients who were not [1]. Despite some dissenting reports [3], it is a more common conclusion that secondary thrombocytosis is not elevated risk of thromboembolic complication, patients with reactive thrombocytosis, developing thrombotic complications, had additional risk factors [4,5]. But in the perioperative period, close observation of whether thromboembolic complication occurs, as well as regular monitoring of platelet count is needed. And possibly, anti-coagulation drug for the patients with additional risk factor may be useful.

Examination of the Relationship Between Antimicrobials and Thrombocytosis

To evaluate whether there is a relationship between antimicrobial therapy and the development of thrombocytosis. Literature was accessed through EMBASE (1977-June 2012) and MEDLINE (1977-June 2012) using the terms thrombocytosis and antimicrobial. In addition, reference citations from publications identified were reviewed. All English-language publications identified were evaluated. For case reports, the Naranjo probability scale was used to calculate the likelihood of the drug causing the reaction. Thrombocytosis occurring during antimicrobial therapy is well documented, with several case reports and clinical trial observations. However, a direct causal relationship is not yet supported by the available literature. Platelets are well known to be an acute phase reactant, with an elevated count occurring after acute conditions such as blood loss, inflammation, or infection. Thrombocytosis during antimicrobial therapy may be the result of an infectious process and not an adverse drug event. Based on the current available literature, a definitive link cannot be established between antimicrobial therapy and occurrence of thrombocytosis.

Development of thrombocytosis in HIV+ drug users: impact of antiretroviral therapy

With the exception of hemolytic anemia, the potential hematological toxicity of antiretrovirals (ARV) and combination treatments in HIV treated individuals has not been well established. We report, for the first time, hematological toxicity defined as thrombocytosis in 9% of the HIV+ patients receiving highly active antiretroviral treatment (HAART) being followed in a nutritional clinical trial. Participants were evaluated every 6 months during a 2-year period (1998-2000) and blood drawn for biochemical, hematological and immunological parameters. NK cells were negatively correlated with platelet counts in the total cohort ( P = 0.018) and persistently elevated with ARVT. Chronic thrombocytosis was associated with significantly lower NK percentages ( P = 0.005). Twenty-five percent of the patients with thrombocytosis developed a cardiovascular disease. Together, these results support the proposal that HAART may increase the risk of hematological dysfunction and impact the risk of cardiovascular disease.

Analysis of Thrombopoietin and c-mpl Expression in a Child with Essential Thrombocythemia

The pathogenesis of the increased number of megakaryocytes and thrombocytosis in essential thrombocythemia (ET) is still unknown. We examined the expression of c-mpl, a receptor of thrombopoietin (TPO), and its signaling molecules in a patient with ET. An 8-year-old girl showed a high platelet count and an increased number of bone marrow megakaryocytes. Neither chromosomal abnormalities nor myelofibrosis was observed. Following the diagnosis of ET, aspirin therapy was begun for the patient, with only modest improvement of symptoms. Her platelet count ranged from 1,200,000/μL to 2,200,000/μL for more than 2years. In the analyses, the serum TPO level in the patient was 420 attomoles/mL (normal, 760 ± 320). The level of c-mpl expression in bone marrow mononuclear cells was higher in the patient than in healthy children, while there was no difference in the level of c-mpl expression in CD34 + cells, indicating an expanded pool of megakaryocytc lineage cells. The level of Janus kinase 2 (Jak2) expression was lower in the patient than in a healthy child. These findings indicate that the signal pathway mediated by c-Mpl after binding to TPO may be impaired in ET. Further analysis is needed to clarify the mechanism underlying the development of thrombocytosis in ET patients.

Platelet count and the outcome of operation for ruptured abdominal aortic aneurysm

The purpose of this study was to determine the relationship between admission and postoperative platelet count (PC) and mortality and morbidity rates after emergency surgery for ruptured abdominal aortic aneurysm (AAA). We performed a case record review of 65 consecutive patients admitted with ruptured AAA. Five patients did not undergo operation because of poor clinical condition, 12 patients died at operation, 13 patients died after operation, and 35 patients survived (operative mortality rate of 58%). Fifteen patients had an admission PC of less than 150 x 10(9)/L, of whom 14 (93%) died; 27 patients had an admission PC of 150 to 250 x 10(9)/L, of whom 8 (30%) died; and 18 patients had an admission PC of greater than 250 x 10(9)/L of whom 3 (17%) died. At the end of operation 29 patients had a PC of less than 100 x 10(9)/L, of whom 13 (45%) died, 20 (69%) had development of multiorgan failure (MOF), and 6 (21%) required relaparotomy for bleeding complications. By contrast, all 19 patients having a PC of 100 x 10(9)/L or greater at the end of the operation survived, three (16%) had development of MOF, and none required further surgery for bleeding. There was a significant inverse correlation between PC at the end of the operation and the number of postoperative days spent on a ventilator, in the intensive therapy unit, and in hospital. After operation, 15 patients had development of thrombocytosis (PC > 400 x 10(9)/L), of whom 10 had development of deep venous thrombosis and 8 had development of pulmonary embolism. There were no deep venous thromboses or pulmonary embolisms in patients who did not have development of a postoperative thrombocytosis. There is a direct correlation between PC on admission to the hospital and death after emergency repair of ruptured AAA. Thrombocytopenia at the end of the operation is associated with a high risk of morbidity from continuing hemorrhage or MOF. The development of postoperative thrombocytosis is associated with a high risk of thromboembolic complications. PC provides a simple marker of outcome in patients diagnosed with and undergoing operation for ruptured AAA.

Antibodies reactive with surface membranes of cellular elements in the blood

Autoreactive antibodies or immune complexes may accelerate clearance of mature erythrocytes, leukocytes, and platelets from the circulation in patients with rheumatologic and immunologic disorders. The most compelling evidence for immune injury to hematopoietic cells exists in patients with systemic lupus erythematosus and patients with Felty's syndrome and its variants. These disorders may also cause tissue inflammation, which in turn commonly results in underproduction of erythrocytes and development of thrombocytosis. However, recent evidence indicates that underproduction of hematopoietic cells may also result from immune injury to cellular elements in the bone marrow. In many laboratories, sensitive techniques are now clinically available for the detection of cell-associated immunoglobulin and complement. These assays have helped confirm the role of antibody in the pathogenesis of autoimmune hemolytic anemia and idiopathic thrombocytopenic purpura. However, recent data indicate that there is probably a continuum between the amount of immunoglobulin and complement found on normal cells and that found in a variety of disease states. In several of these disorders, additional evidence will be required to establish that the increase in cell-bound immunoglobulin leads to a decrease in the life-span of the cell. In order to provide significant help to the clinician managing an individual patient, these serologic tests must be capable of identifying the portion of the cell-associated protein actually involved in the destructive process. The availability of monoclonal reagents capable of identifying restricted regions on cell-bound immunoglobulin may help identify molecules bound specifically as antibody and may help identify the antigens involved in autoimmune disorders.

852 THROMBOCYTOSIS IN PATIENTS WITH SICKLE CELL ANEMIA AND PNEUMONIA

Alterations in platelet function in patients with sickle cell anemia (SCA) may contribute to vaso-occlusive crises. Since thrombocytosis may further enhance thrombotic tendencies, we investigated the occurrence rate, magnitude and adverse effects of thrombocytosis in children with SCA and pneumonia. In 37 patients, 47 episodes of pneumonia were evaluated. Platelet counts in 7 patients rose to greater than 1 × 106/mm3 and in 16 patients to ≥750,000/mm3. The mean platelet count began to rise on the fifth day. From day 7 to day 21 the average platelet count was greater than twice the average count on admission and during asymptomatic periods. There were no platelet aggregation abnormalities detected initially or after the development of thrombocytosis. The mean platelet volumes, determined on an electronic particle counter, also remained constant. Only one patient had a painful crisis during the duration of post-pneumonia thrombocytosis. His painful crisis resolved despite a continued rise in platelet count. Although thrombocytosis following pneumonia in patients with SCA is common, the risk of related vaso-occlusive sequelae appears low and anti-platelet therapy does not appear warranted.