Does Ruxolitinib, in Comparison to Best Available Therapy (BAT), Improve Pruritis Symptoms in Patients with Polycythemia Vera?

Polycythemia vera manifests as a myeloproliferative neoplasm associated with diverse symptoms, including aquagenic pruritis. This systematic review addresses the pressing need to enhance the understanding of the disease’s symptomatology and optimize treatment strategies for improved patient outcomes. The rarity and low prevalence of polycythemia vera underscore the importance of this investigation, as existing standard of care involves a multifaceted approach and significant healthcare costs. Despite advancement in therapeutic options, persistent symptoms and resistance to first-line treatments pose challenges. Ruxolitinib has emerged as a promising intervention, demonstrating clinically significant improvement for patients. This systematic review appraises three randomized controlled trials, shedding light on the efficacy of ruxolitinib and its potential to ameliorate pruritis symptoms in symptomatic patients.

Hemorrhagic transformation after acute ischemic stroke caused by polycythemia vera:Report of two case

BACKGROUNDPolycythemia vera (PV) is a chronic myeloproliferative disorder characterized byan increase in red blood cells in the peripheral blood. Previous work has reportedthe occurrence of thrombosis or hemorrhage arising in the cerebral vasculaturesecondary to PV. However, hemorrhagic transformation after PV-associated acuteischemic stroke has not been previously described.CASE SUMMARYWe herein present two cases of PV where hemorrhagic transformation occurredafter an acute ischemic stroke. Case 1 was a 57-year-old woman with a history ofhypertension who was admitted for left-sided weakness. Case 2 was a 68-year-oldman who was admitted for a 10-d sudden left arm weakness. Imaging examinationsfor the two patients revealed hemorrhagic transformation after acuteischemic stroke. Both patients had JAK-2-V617F mutation and receivedantiplatelet therapy. Both of them had a good prognosis during the follow-up.CONCLUSIONThis report suggested that hemorrhagic transformation may occur in acuteischemic stroke caused by PV. Antiplatelet drugs do not seem to influence thelong-term outcomes in such patients. Future research should focus on establishinga standard antiplatelet treatment strategy for this condition.

Recurrent thrombosis in the lower extremities after thrombectomy in a patient with polycythemia vera:A case report

BACKGROUND Acute arterial embolism of the extremities is a surgical emergency. Atrialfibrillation is the major etiology of acute arterial embolism of the extremities.Emergency femoral artery thrombectomy can successfully treat this issue.However, polycythemia vera (PV) may sometimes explain this medicalemergency. Recurrent thrombosis in the lower extremities after thrombectomycan be found in patients with PV, and reoperation is needed for this condition.CASE SUMMARY A 68-year-old man in China suffered from sudden pain in the left lower extremityfor 14 h. The examination in the emergency department showed a diagnosis ofacute arterial embolism of the extremities combined with PV. The patient’scomplaint disappeared after repeat emergency thrombectomy.CONCLUSION Patients with acute arterial embolism of the extremities should be treatedcarefully, especially those who have recurrent thrombosis after emergencythrombectomy. Clinicians should be aware of PV, a rare cause of acute arterialembolism of the extremities. The combination of thrombectomy, phlebotomy, andantiplatelet and anticoagulant drugs may be a suitable therapeutic regimen forthese patients.

Minimal change disease caused by polycythemia vera: A case report

BACKGROUND Polycythemia vera(PV),often attributed to the JAK2 V617F mutation,is characterized by enhanced red blood cell counts in the peripheral blood.PV-associated renal disease is clinically rare;to date,there have been reports of other chronic kidney diseases related to PV,but no reports on PV-associated minimal change disease.CASE SUMMARY A 37-year-old man presented with proteinuria and high red blood cell count on January 4,2021.The patient underwent bone marrow and renal biopsies,then was subsequently diagnosed with PV and minimal change in disease.Hydroxyurea was administered and proteinuria remission was achieved.The patient’s last visit was on April 14,2022.CONCLUSION We inferred that there may be a causal relationship between PV and minimal change disease.

Recurrent Ischemic Stroke Revealing Polycythemia Vera

Background: Polycythemia vera is a possible cause of recurrent ischemic stroke which can be prevented. Aim: Describe a junctional ischemic stroke without large arterial trunks stenosis associated with an acute coronary syndrome. Case Presentation: A 66-years-old man was admitted for abrupt recurrent right hemiparesis related to bilateral and junctional ischemic stroke lesions. He had a medical history of a vertebrobasilar ischemic stroke concurrent with an acute coronary syndrome with normal coronary arteries. Transthoracic echocardiogram showed small apical akinesia. Hemoglobin level was 18.9 g/dl with a hematocrit of 57.6%. The endogenous erythropoietin was 1.3 mIU/ml with JAK2 V617F mutation positivity (37%). After eight months of treatment (hydroxycarbamide + aspirin + allopurinol) hemoglobin was 12.5 g/dL. Conclusion: This case illustrates the most suggestive features of PV particularly the ischemic stroke junctional topography.

Serum Levels of Testosterone in Patients with Polycythemia Vera

Despite its association with vascular events such as myocardial and cerebral infarction, polycythemia vera (PV) is characterized by low serum total cholesterol levels. Because several sex hormones are derived from cholesterol, statins may induce hypogodanism in male patients. Therefore, we assessed the relationship between serum total cholesterol and sex hormone levels according to gender. Medical records of 41 patients with erythrocytosis (hemoglobin concentrations: men >18.5 g/dL;women >16.5 g/dL) collected between August 2005 and December 2014 were reviewed for patient age, and gender, as well as clinical hematology, biochemistry, and endocrinology laboratory findings. Serum levels of testosterone were lower in men with PV than in patients with reactive erythrocytosis (RE) (PV: 385 ± 78 ng/mL versus RE: 529 ± 46 ng/mL). However, serum levels of testosterone in women with PV were comparable to those in patients in the nonerythrocytic group (PV: 20.5 ± 3.5 ng/mL versus non-erythrocytic group: 21.0 ± 4.3 ng/mL). Serum levels of testosterone were not related to serum levels of cholesterol. Therefore, we speculated that lower testosterone levels were not due to lower serum levels of cholesterol, a known adverse effect of statin. In conclusion, we report for the first time that serum levels of testosterone were lower in male PV patients than in those with RE;however, serum levels of testosterone in female patients with PV were not lower.

Erythrocytosis caused by giant chromophobe renal cell carcinoma:a case report indicating a 9.year misdiagnosis of polycythemia vera

Background:Erythrocytosis,a rare paraneoplastic syndrome,generally occurs in patients with clear cell renal cell carcinoma and has never been reported in patients with chromophobe renal cell carcinoma.Case presentation:We report a case of a young man suffering from a giant(22-cm) mass on his left kidney.Because of a history of polycythemia vera,the patient had been treated for the condition for 9 years.Radical nephrectomy was successfully performed,and the postoperative pathologic examination confirmed a diagnosis of chromophobe renal cell carcinoma.Unexpectedly,the symptom of erythrocytosis disappeared after the surgery.Further examination and analysis were performed,and we finally attributed his erythrocytosis to chromophobe renal cell carcinoma.Conclusions:Chromophobe renal cell carcinoma could cause erythrocytosis,but the clear-cut mechanism needs further research.Secondary erythrocytosis such as those related with renal tumors should be taken into consideration during the diagnosis of polycythemia vera.

Aspirin responsive platelet thrombophilia in essential thrombocythemia and polycythemia vera

Essential thrombocythemia(ET) and polycythemia vera(PV) frequently present with erythromelalgia and acrocyanotic complications, migraine-like microvascular cerebral and ocular transient ischemic attacks(MIAs) and/or acute coronary disease. The spectrum of MIAs in ET range from poorly localized symptoms of transient unsteadiness, dysarthria and scintillating scotoma to focal symptoms of transient monocular blindness, transient mono- or hemiparesis or both. The attacks all have a sudden onset, occur sequentially rather than simultaneously, last for a few seconds to several minutes and are usually associated with a dull, pulsatile or migraine-like headache. Increased hematocrit and blood viscosity in PV patients aggravate the microvascular ischemic syndrome of thrombocythemia to major arterial and venous thrombotic complications. Phlebotomy to correct hematocrit to normal in PV significantly reduces major arterial and venous thrombotic complications, but fails to prevent the platelet-mediated erythromelalgia and MIAs. Complete long-term relief of the erythromelalgic microvascular disturbances, MIAs and major thrombosis in ET and PV patients can be obtained with low dose aspirin and platelet reduction to normal, but not with anticoagulation. Skin punch biopsies from the erythromelalgic area show fibromuscular intimal proliferation of arterioles complicated by occlusive plateletrich thrombi leading to acrocyanotic ischemia. Symptomatic ET patients with erythromelalgic microvascular disturbances have shortened platelet survival, increased platelet activation markers β-thromboglobulin(β-TG), platelet factor 4(PF4) and thrombomoduline(TM), increased urinary thromboxane B2(TXB2) excretion, and no activation of the coagulation markers thrombin fragments F1+2 and fibrin degradation products. Inhibition of platelet cyclooxygenase(COX1) by aspirin is followed by the disappearance and no recurrence of microvascular disturbances, increase in platelet number, correction of the shortened platelet survival times to normal, and reduction of increased plasma levels of β-TG, PF4, TM and urinary TXB2 excretion to normal. These results indicate that platelet-mediated fibromuscular intimal proliferation and platelet-rich thrombi in the peripheral, cerebral and coronary end-arterial microvasculature are responsible for the erythromelalgic ischemic complica-tions, MIAs and splanchnic vein thrombosis. Baseline platelet P-selectin levels and arachidonic acid induced COX1 mediated platelet activation showed a highly significant increase of platelet P-selectin expression(not seen in ADP and collagen stimulated platelets), which was significantly higher in JAK2V617 F mutated compared to JAK2 wild type ET.

Pulmonary vein thrombosis in a patient with polycythemia vera

Pulmonary vein thrombosis(PVT) is a rarely encountered disease entity with varied clinical presentations. It is usually associated with lung carcinoma, lung surgeries and as a complication of the radiofrequency catheter ablation procedure for atrial fibrillation. Its clinical manifestations can vary from mild hemoptysis to lung infarction with hemodynamic compromise. A 76-year-old male presented with a 2-d history of pleuritic left sided chest pain. His past medical history included polycythemia vera, atrial fibrillation, coronary artery disease, pulmonary embolism and pulmonary hypertension. Chest radiograph was normal, troponins were normal and the 12-lead electrocardiogram did not show any ischemic changes. A computerized tomography pulmonary angiogram revealed a filling defect in the left lower lobe pulmonary vein. He was treated with subcutaneous enoxaparin and his symptoms improved. This case highlights a rare etiology of chest pain and the first reported case of the association of polycythemia vera and pulmonary vein thrombosis. A high index of suspicion is required for appropriate diagnostic work up. PVT can mimic pulmonary embolism. The diagnostic work up and treatment strategies depend on acuity of presentation.

Carcinoid tumor of the duodenum and accessory papilla associated with polycythemia vera

Carcinoid tumors have been reported in a wide range of organs but most frequently involve the gastrointestinal tract; however, duodenal carcinoid tumors are rare. We report a 50-year-old male patient complaining of multiple melenas for 3 wk. The panendoscopy and endoscopic retrograde cholangiopancreaticography revealed swelling accessory papilla with an ulcer. The biopsy taken showed a carcinoid tumor. The lesion was removed by wide resection. Patient was found to have an abnormal blood cell count during the follow-up period with elevated levels of hemoglobin and hematocrit of 21.2 g/dL and 63.5%,respectively, thrombocytosis of 501 000/μL, and leukocytosis of 20 410/μL. He was diagnosed as a polycythemia vera by a hematologist after further evaluation. He received periodic phlebotomy and hydroxyurea treatment. The response was good and his hematocrit was stabilized by periodic phlebotomy in the range of 44-49% during the last 2 years. The possible origin of UGI bleeding by a duodenal carcinoid tumor, although rare, should be considered. There has been one case report of a duodenal carcinoid tumor that involved accessory papilla of the pancreas divisum and one case report of metastatic carcinoid tumor associated with polycythemia vera. It is different in our patient as compared with the latter report, which mentioned a polycythemia vera patient who was found to have a metastatic carcinoid in the 17 years follow-up period. Chemotherapy had been given before the carcinoid tumor was revealed. Our patient had no previous chemotherapy for polycythemia vera before he was found to have duodenal carcinoid tumor; this excludes the possibility of chemotherapy induced carcinoid tumor, although it had been suspected in the previous report. In our patient, the existence of both diseases may be by predisposition of each other since both diseases have an increased incidence of other neoplasm, or they may be coexistent incidentally.

Case Report on Feline Polycythemia Vera

Polycythemia vera has been reported as a known condition in cats as early as 1966. This condition manifests as an increased mass in red blood cells and elevated hematocrit and is defined as an idiopathic chronic myeloproliferative disorder. The patient described in this paper presented with hyperemic gums and pinna and an acute onset of progressive ataxia and lethargy. Several possible underlying primary conditions such as cardiac disease and renal malignancy were excluded by running basic blood work and radiographic imaging. Initial blood work revealed a significantly elevated packed cell volume (88%). After diagnosis, treatment with phlebotomy and chemotherapy lead to a reduction in hematocrit and elimination of neurologic signs. This case study represents the diagnosis and successful management of this disease in a private practice setting. Polycythemia vera is relatively uncommon in dogs and cats, but should still be considered in cases of neurologic disorders, especially with the presence of bright red ears, paws, or gums.

Endogenous erythroid colony assay in patients with polycythemia vera and its clinical significance

Background Polycythemia vera (PV) is a malignant disorder of hemaopoietic stem cells which is characterized by clonal hyperproliferation and a low rate of apoptosis. This study was to assess endogenous erythroid colony (EEC) formation in the bone marrow of PV patients and determine its clinical significance Methods The bone marrow mononuclear cells of 26 patients with PV, 2 patients with secondary erythrocytosis (SE), and 19 normal controls were cultured by Marsh's method for EEC evaluation, and the clinical significance was evaluated Results EECs appeared in 25 patients with PV but not in 2 patients with SE and 19 normal controls The number of EECs and the EEC ratio [EEC/erythropoietin (EPO)-dependent colony forming unit-erythroid (CFU-E)] in PV patients positively correlated with hemoglobin (Hb) levels Their EEC number did not correlate with white blood cell (WBC) counts, platelet (PLT) counts, or leukocyte alkaline phosphatase (LAP) scores Their EEC did not correlate with serum EPO levels Fifteen patients with PV were treated with hydroxyurea (Hu) and/or interferon-alpha (IFN-α) Their EEC ratio before treatment positively correlated with the treatment time required for complete remission (CR) and negatively correlated with the time before relapse The EEC numbers of 7 PV patients treated with Hu/IFN-α decreased after the blood cell counts dropped to normal levels There was a positive correlation between the EEC ratio and the incidence of attacks of vascular thrombosis in PV patients The numbers of apoptosised bone marrow mononuclear cells in PV patients were lower than those in normal controls The EEC numbers of PV patients negatively correlated with the rate of apoptosis of bone marrow mononuclear cells Conclusions EEC formation is characteristic in PV patients EEC number in PV patients positively correlates with Hb levels, the time required for CR, and the incidence of attacks of vascular thrombosis EEC number negatively correlates with the time before relapse Bone marrow suppressive treatment might decrease EEC number Thus, EEC number is a sensitive and specific parameter reflecting the abnormal hematopoietic clone burden induced by polycythemia vera EEC number is an important diagnostic parameter for PV patients

Observation of a higher JAK2 V617F homozygous mutated clone in polycythemia vera compared to essential thrombocythemia

Single-tube bi-directional allele specific amp-lification(SB-ASA)and real-time quantitative polymer-ase chain reaction(RQ-PCR)assays were developed and performed for JAK2V617F detection on 40 polycythemia vera(PV)samples,31 essential thrombocythemia(ET)samples,40 acute leukemia samples,and 40 healthy con-trol samples.Differences between detect limitations of the two assays and their influence on the mutation detection rate were analyzed.The results showed that in some sam-ples,the JAK2V617F burden was as low as nearly 1%,and thus more JAK2V617F-positive samples were detected by RQ-PCR than by SB-ASA assay due to the former higher detect limitation.Mutation allele ratios in PV and ET samples and their relevance to biological char-acteristics were also analyzed.The results showed that the mutation allele ratio was 0.436±0.261 in PV,higher than the 0.216±0.207 in ET;percentage of certainly homo-zygous mutation carriers in PV was 40.54%,higher than the 10%in ET.However,statistical analysis showed no relevance between mutation allele burden and sex or age.Our result shows that the pathogenesis of PV and ET may be related to the mutation allele burden of JAK2V617F.

Decreased serum prohepcidin concentration in patients with polycythemia vera

客观的铁缺乏是在有红血球增多症 vera (PV ) 的病人的普通复杂并发症。Hepcidin 是铁动态平衡的一个主要管理者。我们的学习的目的是在 PV 病人的浆液估计 prohepcidin，一位 hepcidin 先锋，和另外的铁地位参数。学习在 60 个病人(F/M 26/34 ) 被执行的方法变老 38 ∼84 (66 ± 1 0 ) 年。控制组由 20 个健康志愿者，匹配的年龄和性别组成了。下列参数在血浆液样品被决定：prohepcidin 集中，熨满意的、不饱和的铁有约束力的能力(UIBC ) ，全部的铁绑定能力(TIBC ) ， transferrin 浸透(TfS ) ，和含铁锡和可溶的 transferrin 受体(sTfR ) 的集中。所有 PV 病人显著地显示出的结果 prohepcidin 的底层，与控制组相比的 sTfR 和 TIBC 高级。从学习组的 40% 病人在正常范围下面并且显著地显示出含铁锡的集中浆液铁和 TfS 的底层，并且与学习组的其余部分比较的 sTfR， UIBC 和 TIBC 显著地高级。在这组病人， prohepcidin 集中是比在另外的病人的那些显著地低的。结果显示那 PV 的结论病人们受不了铁新陈代谢混乱。在 PV 病人的 prohepcidin 的减少的浆液水平可以是铁缺乏的结果。

Myeloproliferative and thrombotic burden and treatment outcome of thrombocythemia and polycythemia patients

Prospective studies indicate that the risk of microvascular and major thrombosis in untreated thrombocythemia in various myeloproliferative neoplasms(MPN-T) is not age dependent and causally related to platelet-mediated thrombosis in early, intermediate and advanced stages of thrombocythemia in MPN-T. If left untreated both microvascular and major thrombosis frequently do occur in MPN-T, but can easily be cured and prevented by low dose aspirin as platelet counts are above 350 × 109/L. The thrombotic risk stratification in the retrospective Bergamo study has been performed in 100 essential thrombocythemia(ET) patients not treated with aspirin thereby overlooking the discovery in 1985 of aspirin responsive platelet-mediated arteriolar and arterial thrombotic tendency in MPN-T disease of ET and polycythemia vera(PV) patients. The Bergamo definition of high thrombotic risk and its persistence in the 2012 International Prognostic Score for ET is based on statistic mystification and not applicable for low and intermediate MPN-T disease burden in ET and PV patients on aspirin. With the advent of molecular screening of MPN patients, MPN-T disease associated with significant leukocytosis, thrombocytosis, constitutional symptoms and/or moderate splenomegaly are candidates for low dose peglyated interferon(Pegasys R, 45 mg/m L once per week or every two weeks) as the first line myeloreductive treatment option in JAK2V617 F mutated MPN-T disease in ET and PV patients. If non-responsive to or side effects induced by IFN, hydroxyurea is the second line myelosuppressive treatment option in JAK2V617 F mutated ET and PV patients with increased MPN-T disease burden.

真性红细胞增多症患者蛋白质组学分析

目的分析真性红细胞增多症患者的蛋白质组学,寻找真性红细胞增多症特异性生物标志物。方法选取2022年1—12月于新乡市第一人民医院就诊的40例真性红细胞增多症患者和40例健康志愿者,分别记作疾病组和健康组。通过高效液相色谱-质谱分析技术筛选出两组受试者血浆表达差异有统计学意义的蛋白;采用Blast2GO数据库对筛选出的差异表达蛋白进行基因本体(GO)和京都基因与基因组百科全书(KEGG)富集分析;采用STRING数据库对差异表达蛋白进行蛋白互作分析。结果健康组和疾病组受试者血浆中共筛选出34种表达差异有统计学意义的蛋白(差异倍数>1.2,P<0.05),与健康组相比较,疾病组患者血浆中有13种蛋白表达上调,21种蛋白表达下调;GO功能富集分析结果显示,两组患者差异表达蛋白主要位于细胞质内,通过干预抗原结合、肽结合、糖胺聚糖结合等分子功能(MF),参与中性粒细胞激活、免疫反应、蛋白级联激活、氧化应激等生物过程(BP);KEGG通路富集分析显示,两组患者差异表达蛋白主要参与了造血细胞谱系、Janus激酶(JAK)/信号转导和转录激活子(STAT)信号通路、细胞黏附分子等代谢途径和信号转导通路;STRING在线数据库分析结果显示,核糖体蛋白S27a(RPS27A)、血红蛋白(Hb)和JAK蛋白与其他蛋白的相关度较高。结论真性红细胞增多症患者差异表达蛋白主要富集于造血细胞谱系、JAK/STAT信号通路、细胞黏附分子等代谢途径和信号转导通路,参与真性红细胞增多症的发生发展,RPS27A、Hb和JAK蛋白可能是诊断真性红细胞增多症的潜在蛋白标志物。

放血疗法联合羟基脲、阿司匹林对真性红细胞增多症患者的影响

目的:探究放血疗法联合羟基脲、阿司匹林治疗真性红细胞增多症患者的效果。方法:选取内蒙古科技大学包头医学院第一附属医院2021年1月—2022年1月收治的60例真性红细胞增多症患者,根据掷硬币法随机分成观察组和对照组,各30例。对照组患者给予羟基脲联合放血疗法治疗,观察组患者在对照组基础上联合小剂量阿司匹林治疗。比较两组临床疗效、凝血功能、血液学指标、不良反应、骨髓增殖性肿瘤总症状评估量表(MPN-SAF-TSS)评分及血栓发生率。结果:观察组治疗总有效率较对照组更高,血栓发生率较对照组更低(P<0.05)。治疗前,两组凝血功能指标比较,差异均无统计学意义(P>0.05);治疗后,两组活化部分凝血活酶时间(APTT)、凝血酶原时间(PT)、凝血酶时间(TT)较治疗前均有所延长,且观察组的APTT、PT、TT均较对照组更长,两组纤维蛋白原(FIB)水平均降低,且观察组FIB水平显著低于对照组(P<0.05)。治疗前,两组红细胞(RBC)、血红蛋白(Hb)、血小板计数(PLT)、白细胞(WBC)水平比较,差异均无统计学意义(P>0.05);治疗后,两组RBC、Hb、PLT、WBC水平均有所降低,且观察组RBC、Hb、PLT、WBC水平均显著低于对照组(P<0.05)。治疗后,观察组MPN-SAF-TSS评分低于对照组(P<0.05)。两组不良反应发生率比较,差异无统计学意义(P>0.05)。结论:放血疗法联合羟基脲、阿司匹林治疗真性红细胞增多症,不仅可以改善患者的凝血功能和血液学指标,而且能够提高治疗效果,降低患者的血栓发生率,且不增加不良反应。

Budd-Chiari syndrome in myeloproliferative neoplasms:A review of literature

Myeloproliferative neoplasms(MPNs)are defined as clonal disorders of the hematopoietic stem cell in which an exaggerated production of terminally differentiated myeloid cells occurs.Classical,Philadelphia-negative MPNs,i.e.,polycythemia vera,essential thrombocythemia and primary myelofibrosis,exhibit a propensity towards the development of thrombotic complications that can occur in unusual sites,e.g.,portal,splanchnic or hepatic veins,the placenta or cerebral sinuses.The pathogenesis of thrombotic events in MPNs is complex and requires an intricate mechanism involving endothelial injury,stasis,elevated leukocyte adhesion,integrins,neutrophil extracellular traps,somatic mutations(e.g.,the V617F point mutation in the JAK2 gene),microparticles,circulating endothelial cells,and other factors,to name a few.Herein,we review the available data on Budd-Chiari syndrome in Philadelphia-negative MPNs,with a particular focus on its epidemiology,pathogenesis,histopathology,risk factors,classification,clinical presentation,diagnosis,and management.

Acute myocardial infarction in myeloproliferative neoplasms

Myeloproliferative neoplasms(MPNs)are a heterogeneous group of hematologic malignancies characterized by an abnormal proliferation of cells of the myeloid lineage.Affected individuals are at increased risk for cardiovascular and thrombotic events.Myocardial infarction(MI)may be one of the earliest clinical manifestations of MPNs or may be a thrombotic complication that develops during the natural course of the disease.In the present review,we examine the epidemiology,pathogenesis,clinical presentation,and management of MI in MPNs based on the available literature.Moreover,we review potential biomarkers that could mediate the MI-MPNs crosstalk,from classical biochemical tests,e.g.,lactate dehydrogenase,creatine kinase and troponins,to pro-inflammatory cytokines,oxidative stress markers,and clonal hematopoiesis.

Risk of hepatitis B reactivation in patients with myeloproliferative neoplasms treated with ruxolitinib

Classical Philadelphia-negative myeloproliferative neoplasms(MPNs),i.e.,polycythemia vera,essential thrombocythemia,and primary/secondary myelofibrosis,are clonal disorders of the hematopoietic stem cell in which an uncontrolled proliferation of terminally differentiated myeloid cells occurs.MPNs are characterized by mutations in driver genes,the JAK2V617F point mutation being the most commonly detected genetic alteration in these hematological malignancies.Thus,JAK inhibition has emerged as a potential therapeutic strategy in MPNs,with ruxolitinib being the first JAK inhibitor developed,approved,and prescribed in the management of these blood cancers.However,the use of ruxolitinib has been associated with a potential risk of infection,including opportunistic infections and reactivation of hepatitis B.Here,we briefly describe the association between ruxolitinib treatment in MPNs and hepatitis B reactivation.