重症酒精性肝炎进展为慢加急性肝衰竭的危险因素

目的 探讨重症酒精性肝炎(severe alcoholic hepatitis,SAH)患者住院期间发生慢加急性肝衰竭(acute-on-chronic liver failure,ACLF)的危险因素。方法 回顾性收集2008年8月至2017年10月首都医科大学附属北京地坛医院诊断为SAH的258例住院患者为研究对象,根据住院期间是否发生ACLF分为ACLF组(84例)和无ACLF组(174例),比较两组患者的临床资料、血常规[白细胞总数(white blood cell,WBC)、血小板(platelet,PLT)、血红蛋白(hemoglobin,HGB)、红细胞平均体积(mean corpuscular volume,MCV)]、肝功能[丙氨酸氨基转移酶(alanine aminotransferase,ALT)、天门冬氨酸氨基转移酶(aspartate aminotransferase,AST)、总胆红素(total bilirubin,TBil)、γ-谷氨酰转移酶(gamma-glutamyl transpeptidase,GGT)、白蛋白(albumin,ALB)]、肾功能...     

CLIF-C OFs在乙型肝炎相关慢性肝病急性失代偿患者中鉴别慢加急性肝功能衰竭的临床研究

目的探究欧洲肝病学会提出的适用于以酒精为病因引起的慢加急性肝衰竭诊断标准(CLIF Consortium Organ Failure score,CLIF-C OF)是否适用于乙型肝炎相关的慢加急性肝衰竭。方法筛选并纳入2005年1月至2010年12月上海瑞金医院乙型肝炎相关慢性肝病急性失代偿患者854例,按CLIF-C OF标准分为ACLF组和非ACLF组。分析ACLF组和非ACLF组的临床和实验室指标、病情严重程度和短期病死率。结果 ACLF组262例和非ACLF组592例。ACLF组较非ACLF组年龄大,肝、肾、脑、凝血、循环、呼吸功能衰竭情况均显著高于入院非ACLF组(P0.01),28 d和90 d病死率均显著升高(27.1%比3.1%、39.6%比4.9%,P0.01),提示病情更重。结论欧洲肝病学会所提出的评分标准可从乙型肝炎相关慢性肝病合并急性失代偿患者中筛选出一组病情更为危重、病死率更高的慢加急性肝衰竭患者群体。乙型肝炎相关慢性肝病并发急性失代偿患者中确实存在一群疾病程度更严重的ACLF群体,CLIF-C OF标准可将ACLF患者从乙型肝炎相关慢性肝病并发急性失代偿患者中区分出来,以指导临床医生治疗决策。     

Recombinant human thrombopoietin attenuates carboplatin-induced severe thrombocytopenia and the need for platelet transfusions in patients with gynecologic cancer

BACKGROUND: Thrombocytopenia is a significant problem in the treatment of cancer. OBJECTIVE: To assess the clinical safety of therapy with recombinant human thrombopoietin (rhTPO) and its ability to ameliorate chemotherapy-induced severe thrombocytopenia. DESIGN: Phase I/II clinical cohort study. SETTING: The University of Texas M.D. Anderson Cancer Center, Houston, Texas. PATIENTS: 29 patients with gynecologic cancer. INTERVENTION: Recombinant human thrombopoietin was given before chemotherapy and after a second cycle of carboplatin therapy. MEASUREMENTS: Peripheral blood counts and platelet transfusions. RESULTS: Administration of rhTPO after chemotherapy significantly reduced the degree and duration of thrombocytopenia and enhanced platelet recovery. In patients who received the optimal biological dose of rhTPO (1.2 microg/kg of body weight) in cycle 2 (carboplatin plus rhTPO), the mean platelet count nadir was higher (44x10(9) cells/L and 20x10(9) cells/L; P = 0.002) and the duration of thrombocytopenia was shorter (days with a platelet count <20x10(9) cells/L, 1 and 4 [P = 0.002]; days with a platelet count <50x10(9) cells/L, 4 and 7 [P = 0.006]) than in cycle 1 (carboplatin only). The need for platelet transfusion in this group was reduced from 75% of patients in cycle 1 to 25% of patients in cycle 2 (P = 0.013). CONCLUSIONS: Therapy with rhTPO seems to be safe and may attenuate chemotherapy-induced severe thrombocytopenia and reduce the need for platelet transfusions.     

Efficacy and safety of linezolid in liver transplant patients

S. Radunz, B. Juntermanns, G.M. Kaiser, J. Treckmann, Z. Mathe, A. Paul, F.H. Saner. Efficacy and safety of linezolid in liver transplant patients
Transpl Infect Dis 2011: 13: 353–358. All rights reserved Abstract: Bacterial infections are the main cause of death within the first year after liver transplantation, and the increased incidence of multidrug‐resistant gram‐positive pathogens has created a major challenge in the treatment of these patients. Linezolid, the first US Food & Drug Administration‐approved oxazolidinone, offers a valuable novel treatment option for serious gram‐positive infections. Linezolid is relatively non‐toxic but prolonged treatment with linezolid was associated with thrombocytopenia. Here we report on the experience of linezolid treatment in adult liver transplant patients, who are at an increased risk for thrombocytopenia because of hypersplenism. From November 2003 until December 2009, we evaluated the clinical course of 46 liver transplant patients (27 male/19 female) in our surgical intensive care unit. For proven or probable gram‐positive infection, all patients received linezolid 600 mg intravenously every 12 h. On clinical improvement, treatment was changed to oral linezolid 600 mg twice daily. Treatment duration was 11 ± 7 days. Treatment indications were pneumonia (n=8), blood stream infection (n=30), and surgical site/abdominal infection (n=3). Clinical cure was achieved in 43 out of 46 patients. During the course of treatment, no cases of severe thrombocytopenia occurred and a statistically significant platelet count increase was seen from day 1 (110 ± 73/nL) to day 7 (165 ± 116/nL) and day 14 (180 ± 140/nL). We did not observe any further adverse events, especially no severe neurological complications (e.g., serotonin syndrome) or signs of lactate acidosis. Two patients died from uncontrolled vancomycin‐resistant Enterococcus faecium sepsis with septic shock and one due to uncontrolled methicillin‐resistant Staphylococcus aureus pneumonia. These deaths were considered to be unrelated to linezolid treatment, and linezolid was regarded as the optimal treatment choice in these patients. A subgroup analysis of patients treated for >14 days revealed no statistically significant differences when compared with patients on shorter treatment. In particular, no cases of thrombocytopenia occurred during longer treatment. In conclusion, linezolid is a safe and effective treatment for adult liver transplant patients with gram‐positive infections.     

Incidence and prognostic significance of thrombocytopenia in patients treated with prolonged heparin therapy

BACKGROUND: Despite widespread heparin use in clinical practice, the associated development of thrombocytopenia is an underrecognized and undertreated complication. METHODS: We analyzed data from consecutive hospitalized patients treated with heparin (unfractionated or low molecular weight) for 4 days or longer to determine the incidence, predictors, prognostic significance, and management of "thrombocytopenia," defined as a platelet count less than 150 x 10(9)/L, reduction in platelet count of 50% or more from the admission level, or both. RESULTS: We enrolled 2420 patients (median age, 65.2 years; 43.8% women) in 48 US hospitals. Thrombocytopenia occurred in 881 patients (36.4%; 95% confidence interval [CI], 34.5%-38.3%). Of those who developed thrombocytopenia, 5.1% died, compared with 1.6% of those without thrombocytopenia (odds ratio [OR], 3.4; 95% CI, 2.1-5.6; P< .001). Thrombocytopenia was also associated with greater risk of myocardial infarction (OR, 2.1; 95% CI, 1.5-2.8; P< .001) and congestive heart failure (OR, 1.3; 95% CI, 1.1-1.6; P= .01). After adjustment for important covariates, thrombocytopenia remained an independent predictor of thrombotic and hemorrhagic events. A relative reduction in platelet count of more than 70% was the strongest independent predictor of death (OR, 13.4; 95% CI, 6.5-27.6; P< .001), followed by a relative reduction in platelet count of 50% to 70%, worse Killip class, occurrence of thromboembolic complications, older age, and longer duration of heparin therapy. CONCLUSIONS: Thrombocytopenia occurs frequently after prolonged heparin therapy and is strongly associated with worse short-term clinical outcome. The relative reduction in platelet count is a powerful independent predictor of all-cause mortality in hospitalized patients.     

Anti-Helicobacter pylori seropositivity: influence on severity and treatment response in patients with chronic hepatitis C

We sought to clarify the incidence and role of Helicobacter pylori (H. pylori) seropositivity in patients with hepatitis C virus (HCV) infection and the effect of coinfection on interferon-alpha and ribavirin therapy. The presence of H. pylori was tested using a commercially available enzyme immunoassay in serum samples from 93 patients with chronic hepatitis C. Clinical features, HCV markers and response of HCV to interferon-alpha and ribavirin were compared between H. pylori-positive and H. pylori-negative patients. Anti-H. pylori antibody was detected in 45 (48%) of the 93 patients, whose median HCV-RNA level (495 vs 760 kIU/mL; P = 0.013) and platelet count (128 vs 158 x 10(3)/microL; P = 0.009) were significantly lower than in patients with HCV infection alone. Anti-H. pylori antibody levels were found to be significantly correlated with fibrosis score (P = 0.0083, r = 0.33) but inversely related to platelet count (P = 0.0037, r = -0.34). The sustained response rate for HCV clearance following interferon-alpha and ribavirin treatment did not differ between patients with and without anti-H. pylori seropositivity. The presence of H. pylori [odds ratio (OR) 8.61; 95% confidence interval (CI) 1.59-46.70] and fibrosis score (OR 30.13; 95% CI 5.44-166.78) were found by multivariate analysis to be associated with the decrease of platelet count during therapy. Coexistent H. pylori infection does not demonstrably influence the clinical course of chronic hepatitis C. A possible connection between H. pylori coinfection and thrombocytopenia was found during the treatment course, suggesting that preemptive eradication of H. pylori may facilitate completion of treatment and increased sustained virological response.     

肝硬化食管胃底静脉曲张破裂出血伴缺血性肝炎的危险因素分析

目的探讨肝硬化食管胃底静脉曲张破裂出血(esophageal and gastric varices bleeding,EGVB)继发缺血性肝炎的相关危险因素。方法回顾性分析2020年1月至8月沈阳市第六人民医院102例EGVB患者的临床资料,根据是否出现缺血性肝炎分为观察组和对照组。对一般资料、实验室指标、辅助检查结果、临床情况进行单因素分析,二元Logistic多因素分析EGVB后继发缺血性肝炎的相关危险因素。结果102例EGVB患者中,14例伴有缺血性肝炎(转氨酶升高>10倍正常值上限)纳入观察组,余88例纳入对照组。观察组死亡5例,是对照组的4.46倍。观察组ALT、AST峰值多出现在入院第2日,依次为791.00(555.25,1657.5)U/L、2541.50(1480.50,4594.00)U/L。单因素分析结果显示,观察组和对照组ALT、AST、γ-GGT、LDH、TBil、白细胞、血小板计数、脾长、脾门静脉、门脉主干内径、门静脉血栓、死亡、合并肝性脑病、合并脓毒症、Child-Pugh评分、腹腔积液等指标,差异有统计学意义(均P<0.05);二元logistic多因素分析显示,伴有肝癌(P<0.01)、白细胞计数(P=0.014)、γ-GGT(P=0.025)、Child-Pugh分级(P=0.050)与EGVB后出现缺血性肝损伤具有显著相关性。结论伴有肝癌、白细胞计数、肝硬化Child-Pugh分级是EGVB合并缺血性肝炎的危险因素。     

Mechanisms of thrombocytopenia in patients with lymphoproliferative diseases.

Different factors are involved in the development of thrombocytopenia in patients with lymphoproliferative disorders. Significant correlation was detected between the number of megakaryocytes in bone marrow and platelet count (r = 0.485, p = 0.002, n = 37) and significant difference between the number of megakaryocyte in patients with normal platelet count (> 200,000/microliters) and patients with marked thrombocytopenia (platelet count < 100,000/microliters). All patients in the latter group (n = 15) had a relatively low number of megakaryocytes. Low but significant reverse correlation was found between the level of platelet-associated IgG (PA-IgG) and platelet count (r = -0.249, p = 0.024, n = 82) and significant difference between the mean levels of PA-IgG in the groups of patients with platelet count > 200,000/microliters and < 100,000/microliters. PA-IgG were increased in 46% of patients in the total group and in 65% of patients with platelet count < 100,000/microliters. The correlation between platelet count and PA-IgG was about 2 times higher in splenectomized (r = -0.549, p = 0.005, n = 24) than nonsplenectomized patients. All splenectomized patients with platelet count < 100,000/microliters (n = 8) had a significant increase in PA-IgG. Serum antibodies were detected in only 7% of tested patients. This group was characterized by severe thrombocytopenia (in 6 of 10 patients--platelet count < 50,000/microliters) and a high incidence of haemorrhages (in 5 of 10 patients). Thus the depression of platelet production was suggested to be the basic cause of thrombocytopenia in lymphoproliferative disorders. Involvement of immune mechanisms was revealed in a large number of patients and correlated with a deeper and more complicated thrombocytopenia.     

Clinical course of thrombocytopenia in patients treated with imatinib mesylate for accelerated phase chronic myelogenous leukemia

We studied 28 patients with accelerated phase chronic myelogenous leukemia (CML) who were enrolled on the Novartis expanded access study 114. Diagnosis of accelerated phase CML was based on karyotypic evolution (n = 9) and hematologic criteria (n = 18). All patients were begun on 600 mg/day of imatinib mesylate. Dose reductions to 400 mg/day and then 300 mg/day were prescribed for an absolute neutrophil count (ANC) of <0.5/microl or a platelet count of <20,000/microl. Twenty-seven of the 28 patients continued treatment for a median of 34 weeks. Eleven patients developed thrombocytopenia following an average of 8.4 +/- 1.4 weeks of therapy. The onset of thrombocytopenia was associated with disease progression in one patient and a decline in bone marrow megakaryocytes in the other 10. Nine patients recovered to a platelet count of >20,000/microl after an average of 19.7 +/- 1.8 weeks. Patients who developed thrombocytopenia had a longer duration of disease (9.39 vs. 4.35 years; P < 0.01) and were more likely to be diagnosed with accelerated phase CML by hematologic criteria. Hematologic responses in patients with and without thrombocytopenia were comparable; however, 31.3% of patients without thrombocytopenia had a complete cytogenetic response compared to none of those with thrombocytopenia. Grade III-IV thrombocytopenia is common in accelerated phase CML and may be a marker for the inability to achieve cytogenetic response using single agent imatinib mesylate.     

Thrombopoietin concentrations are low in patients with cirrhosis and thrombocytopenia and are restored after orthotopic liver transplantation

BACKGROUND: Thrombocytopenia in cirrhotic patients may be due to deficient production of thrombopoietin. AIMS: To determine the relation between thrombopoietin and thrombocytopenia in cirrhotic patients before and after orthotopic liver transplantation. METHODS: Thrombopoietin concentrations and platelet counts were measured in 43 cirrhotic patients and 21 normal controls and serially for 14 days after transplantation in 23/43 patients. RESULTS: 27 of the 43 patients had thrombocytopenia (platelet count less than 120 x 10(9)/l; group 1) whereas 16 patients had normal platelet count (group 2). Thrombopoietin concentrations were lower in group 1 than in group 2 (92.5 (20.3-286.3) v 226.6 (30.1-848.3) pg/ml, p=0.003) and normal controls (92.5 (20.3-286.3) v 158.3 (22.5-232.9) pg/ml, p=0.028). Post-transplantation thrombopoietin concentrations increased with a peak at day 5. The rise was significant in patients with low pretransplantation platelet count (89.1 (21.29-247.6) to 545.1 (66.2-2569) pg/ml; n=16, p=0.001) but not in those with normal platelet count (262.8 (30.1-848.3) to 315.1 (114-954.6) pg/ml; n=7, p=0.47). No correlation was found pretransplantation between spleen volume and platelet count (r=-0.11, p=0.6) or thrombopoietin concentrations (r=-0.04, p=0.8). However, pretransplantation thrombopoietin concentrations correlated with platelet count (r=0.47, p=0.0015), whereas an inverse correlation was found between peak thrombopoietin concentrations and nadir platelet count (r=-0.41 p=0. 049) post-transplantation. CONCLUSIONS: Inadequate thrombopoietin production may contribute to cirrhotic thrombocytopenia. Thrombopoietin production is restored after liver transplantation leading to the resolution of thrombocytopenia.     

Granulocyte-colony stimulating factor therapy improves survival in patients with hepatitis B virus-associated acuteon-chronic liver failure

AIM:To evaluate the safety and efficacy of granulocyte-colony stimulating factor(G-CSF) therapy in patients with hepatitis B virus(HBV)-associated acuteon-chronic liver failure(ACLF).METHODS:Fifty-five patients with HBV-associated ACLF were randomized into two groups:the treatment group and the control group.Twenty-seven patients in the treatment group received G-CSF(5 μg/kg per day,six doses) treatment plus standard therapy,and 28 patients in the control group received standard therapy only.The peripheral CD34 + cell count was measured consecutively by flow cytometry.Circulating white blood cell count,biochemical parameters,and other clinical data of these patients were recorded and analyzed.All patients were followed up for a period of 3 mo to evaluate the changes in liver function and survival rate.RESULTS:The peripheral neutrophil and CD34 + cell counts in the G-CSF group increased on day 3 from the onset of therapy,continued to rise on day 7,and remained elevated on day 15 compared to those of the control group.Child-Turcotte-Pugh score of patients in the treatment group was improved on day 30 from the onset of G-CSF therapy,compared to that in the controls(P = 0.041).Model for End-Stage of Liver Disease score of patients in the treatment group was improved on day 7(P = 0.004) and remained high on day 30 from the onset of G-CSF therapy(P < 0.001) compared to that in controls.After 3 mo of follow-up observation,the survival rate in the treatment group(48.1%) was significantly higher than that in the control group(21.4%)(P = 0.0181).CONCLUSION:G-CSF therapy promoted CD34 + cell mobilization in patients with HBV-associated ACLF,and improved the liver function and the survival rate of these patients.     

Factors linked to severe thrombocytopenia during antiviral therapy in patients with chronic hepatitis c and pretreatment low platelet counts

Background  

Baseline low platelet count (< 150,000/μL) increases the risk of on-treatment severe thrombocytopenia (platelet count < 50,000/μL) in patients with chronic hepatitis C (CHC) undergoing antiviral therapy, which may interrupt treatment. The purpose of this study was to identify risk factors for severe thrombocytopenia during treatment for CHC in patients with baseline thrombocytopenia.     

HIV/AIDS合并血小板减少患者HAART后血小板复常的特征及影响因素分析

目的分析HIV/AIDS合并血小板减少患者在高效抗逆转录病毒治疗(highly active antiretroviral therapy,HAART)后血小板的复常特征,探讨影响复常的相关因素。方法采用回顾性分析,以2003年6月—2015年12月在北京地坛医院进行抗病毒治疗的132例HIV/AIDS合并血小板减少的患者为研究对象,分析患者HAART 4周和24周后血小板的复常率及基本特征。结果 1 132例患者中血小板轻度减少99例(75.00%),中度减少19例(14.39%),重度减少14例(10.61%)。患者HAART 4周、24周后血小板的复常率分别为63.9%、80.8%,差异具有统计学意义(P=0.003)。2单因素Logistic分析提示通过血液传播(OR=4.632,P=0.024),合并HBs Ag阳性(OR=3.829,P=0.024)及合并抗HCV阳性(OR=6.476,P=0.020)是影响血小板复常的因素,多因素Logistic分析提示合并HBs Ag阳性(OR=4.345,P=0.027)是影响血小板复常的因素。结论 HAART为HIV/AIDS合并血小板减少最有效的方法,尽早HAART可避免血小板持续降低。HBs Ag阳性是影响血小板复常的主要因素。对于存在危险因素的患者应该给予重视,尽早做出干预措施。     

低分子肝素治疗高原老年急性冠状动脉综合征患者的临床研究

目的观察低分子肝素治疗高原老年急性冠脉综合征（ACS）患者的疗效及安全性。方法将90例老年ACS患者随机分为常规治疗组（n=42）和延长低分子肝素治疗组（n=48）,常规治疗组采用低分子肝素（依诺肝素）皮下注射治疗5～7d,延长低分子肝素治疗组治疗10～14d,其余基础治疗相同。观察30d内心血管事件、出血事件和血小板减少的发生率。结果常规治疗组30d内心血管事件的发生率为19．0％,延长治疗组为4．2％,两组间差异有统计学意义（P〈0．05）;常规治疗组30d内出血事件的发生率为4．8％,延长治疗组为6．3％,两组间差异无统计学意义（P〉0．05）;两组患者中均未观察到血小板减少的发生。结论延长使用（10～14d）低分子肝素治疗高原老年ACS可显著降低30d内心血管事件的发生率,且不增加出血风险和血小板减少事件的发生率。     

前瞻性研究四种出血事件评估标准评估慢加急性肝衰竭患者出血事件*

目的 探讨应用常用的四种出血事件评估标准判断慢加急性肝衰竭（ACLF）患者出血事件。方法 在56例非-ACLF、26例达到亚太肝病协会发布标准的ACLF（APASL-ACLF）和12例达到欧洲肝病学会（EASL）发布的ACLF（EASL-ACLF）患者,采用出血学术研究会标准（BARC）、心肌梗死溶栓标准（TIMI）、开通闭塞冠状动脉策略的全球性研究标准（GUSTO）和国际血栓与止血委员会标准（ISTH）分别进行量化评分,观察28 d和90 d生存情况。结果 本组57.6%患者在住院期间发生出血事件,致死性出血事件发生率为1.1%;非ACLF组出血发生率为41.1%,显著低于APASL-ACLF组或EASL-ACLF组的76.9%和100.0%（P<0.05）;有出血事件组28 d和90 d病死率分别为13.0%和24.5%,显著高于无出血组的0.0%和 0.0%（P<0.01）;BARC标准、TIMI标准和GUSTO标准判断28 d短期预后的受试者工作特征曲线（ROC）下面积（AUC）分别为0.880（95%CI：0.747~1.000）、0.801（95%CI：0.653~0.94）和0.841（95%CI：0.697~0.984）,均显著低于ISTH标准的0.95（95%CI：0.861~1.000,P<0.05）。结论 ACLF患者出血事件发生率较高,随着疾病严重程度增加而增多,但致死性出血事件少见。在四种出血评分标准中,经验证,ISTH标准适用性最好。     

Thrombokinetics in patients with rheumatoid arthritis treated with D-penicillamine.

The mechanism of D-penicillamine induced thrombocytopenia in rheumatoid arthritis was investigated by measuring platelet life-span and platelet production rate in 2 groups of rheumatoid arthritis patients treated with 250-750 mg/day D-penicillamine, 14 with a normal platelet count and 9 with thrombocytopenia (platelet count 50-130 X 10(9)/1). Age matched control patients not treated with D-penicillamine included 14 with rheumatoid arthritis and 9 with osteoarthritis. The platelet life-span was normal, but platelet production rate was significantly reduced in the thrombocytopenic patients, suggesting that D-penicillamine causes thrombocytopenia through bone marrow suppression.     

Characteristics of type I Gaucher disease associated with persistent thrombocytopenia after treatment with imiglucerase for 4-5 years

The characteristics of Gaucher disease (GD) associated with persistent thrombocytopenia despite imiglucerase enzyme therapy in type 1 GD (GD1) were investigated by retrospective analysis of International Collaborative Gaucher Group (ICGG) Registry data. The study involved 1016 GD1 patients with an intact spleen for whom date of diagnosis, therapy initiation, and platelet counts were known, and who received continuous imiglucerase therapy for 4 to 5 years. These patients were stratified by last platelet count: ≥ 120 × 10(9) /l (n = 772); ≥ 100 to <120 × 10(9) /l (n = 94); ≥ 80 to <100 × 10(9) /l (n = 80); and <80 × 10(9) /l (n = 70; 20 with <60 × 10(9) /l) and characterized by initial and cumulative average imiglucerase dose, body mass index, platelet count, anaemia, hepatomegaly, splenomegaly, and skeletal assessments at baseline and after 4-5 years of therapy. Statistically significant associations were found between persistent thrombocytopenia and baseline platelet count (<80 × 10(9) /l), splenomegaly, and anaemia (all P < 0·0001). After 4-5 years, statistically significant associations were found with splenomegaly (P < 0·0001), anaemia (P < 0·0001), white blood cell count (P = 0·049), hepatomegaly (P = 0·004) and bone pain (P = 0·035). Exponential platelet decay in relation to splenomegaly suggests that platelets increase only when spleen volume decreases substantially.     

Intravenous gammaglobulin treatment for immune thrombocytopenia associated with infectious mononucleosis

Severe thrombocytopenia is an uncommon (incidence less than 1%) but serious complication of infectious mononucleosis. Corticosteroids have been used for therapy with variable responses reported. Five consecutive patients with infectious mononucleosis-related severe thrombocytopenia were treated with intravenous gammaglobulin (IVIG) at a dose of 400 mg/kg/day for 2-5 days. All patients appear to have had an immunologic or consumptive etiology for their thrombocytopenia as determined by increased marrow megakaryocytes. All patients were initially treated with oral prednisone 1 mg/kg/day. Due to the relatively slow response to prednisone (platelet count less than 20,000/microliters on the 8th to 13th hospital day) or increased bleeding symptoms, IVIG was initiated. Four of the five patients rapidly developed significant increases in their platelet counts (range 44,000/microliters to 97,000/microliters). Two of these responses were sustained and two relapses occurred (while on continued steroid therapy) which again responded to booster doses of IVIG at similar doses. IVIG has been previously shown to be effective in treating patients with idiopathic thrombocytopenia purpura. Historically, patients with infectious mononucleosis-related severe thrombocytopenia often are refractory to corticosteroid therapy and our limited experience suggests that IVIG may also be effective in infectious mononucleosis-related severe thrombocytopenia.     

Thrombocytopenia in patients treated with heparin, combination antiplatelet therapy, and intra-aortic balloon pump counterpulsation

Objectives: Determine the incidence and timing of intra-aortic balloon pump (IABP)-associated thrombocytopenia, if concomitant antiplatelet agents increase the incidence of thrombocytopenia, and the incidence of heparin-induced thrombocytopenia (HIT) in a contemporary IABP population.
Background: Previous studies predate the current practice of treating acute coronary syndrome patients with heparin and aspirin plus thienopyridines and glycoprotein IIb/IIIa receptor antagonists such that data are unavailable to determine if their co-administration worsens IABP-associated thrombocytopenia.
Methods: A retrospective cohort study of adult IABP patients (n = 107) from 2002 to 2006 was performed to determine the indication for and duration of counterpulsation, platelet counts during and for 7 days postcounterpulsation, medications potentially contributing to thrombocytopenia, and HIT antibody results if obtained.
Results: Thrombocytopenia, defined as platelets <150,000/mL or >50% decrease from baseline, occurred in 57.9% of patients. Overall, platelets declined to 60.2 ± 22.8% of baseline with the mean (± standard deviation) nadir on day 2.8 ± 2.0. Comparing patients who received heparin, aspirin, thienopyridines, and glycoprotein IIb/IIIa antagonists (n = 44) versus heparinized patients ± aspirin (n = 45), platelet nadirs were 62.7 ± 20.9% versus 58.3 ± 23.9% of baseline levels, respectively (P = 0.42). The incidence of HIT was 2.8% in the entire cohort.
Conclusions: IABP-associated thrombocytopenia occurred in 57.9% of this cohort. HIT was diagnosed in 2.8% and should be considered as a diagnosis if platelet counts do not stabilize or continue to fall after 3–4 days of counterpulsation. Increased use of antiplatelet therapy does not impact the degree of thrombocytopenia although the current practice of prompt IABP removal may offset this effect.     

Pre-procedural use of thrombopoietin-receptor agonists in cirrhosis and severe thrombocytopenia: A systematic review and meta-analysis

BackgroundSevere thrombocytopenia in cirrhosis can preclude invasive procedures. Platelet transfusion is recommended if platelet count pre-procedure is potential alternative to platelet transfusion is thrombopoietin-receptor (TPO) agonists.AimEvaluate TPO-agonist efficacy and safety in cirrhotic patients with severe thrombocytopenia undergoing invasive procedures.MethodsRandomized control trials (RCT) from electronic reference databases were searched from inception till December 2019. PRISMA guidelines were followed. Primary outcome was platelet transfusion avoidance. Secondary outcomes were weighted mean difference (WMD) in platelet count from baseline to pre-procedure and rates of major adverse events (AE). Pooled Odds Ratio (OR) were estimated using a random-effects model.ResultsSix RCTs with 1,229 patients were included. All studies had low risk of bias.Compared with placebo, those treated with TPO-agonists had a pooled OR of 0.12(0.08-0.17), P<0.01 for platelet transfusion avoidance, and WMD in platelet count (x10 3 /µL) of 35.6(28.6-42.7), P<0.01. Major AE did not differ between groups [Pooled OR: 0.87(0.47–1.62), P=0.66].ConclusionCompared to placebo, TPO-agonists used in cirrhotic patients with severe thrombocytopenia prior to elective invasive procedures had 88% reduced odds of requiring peri-procedural platelet transfusion and increased platelet count pre-procedure, with no difference in AE rates.