中图分类号:
R994.1R979.1
文献标识码:
B
文章编号:
1004-0781(2021)04-0551-05
摘要:
目的 探讨伊沙佐米所致不良反应(ADRs)的发生情况和临床特点,为临床合理用药提供参考。方法 检索伊沙佐米2015年11月上市以来中国学术期刊全文数据库(CNKI)、维普中文科技期刊数据库(VIP)、Pubmed、Medline、Web of Science数据库收载的不良反应文献,进行统计分析。结果 伊沙佐米致ADRs的个案报告共10例;其年龄分布以61~80岁年龄段较多(7例);多发生用药后6周内(8例);以皮肤及附件损害(5例)、血液系统损害(2例)多见,且出现了新的严重不良反应,如血栓性微血管病(TMA)、进行性多灶性白质脑病(PML)、急性胰腺炎(AP)和心脏毒性。结论 临床医师和药师需加强对伊沙佐米致ADRs的认识和监测,尤其是新的严重ADRs,谨慎评估再次给药的治疗风险,保证临床用安全、有效。
关键词:
伊沙佐米
;
不良反应
;
文献分析
Abstract:
Objective To analyze the status and characteristics of adverse drug reactions(ADRs)induced by ixazommib,and to provide references for the clinical medication. Methods ADRs of ixazommib reported by medical science journals were collected and analyzed statistically from CNKI,VIP,Pubmed,Medline,and Web of Science database from Nov.2015 to Jan.2020. Results A total of 10 ADRs were identified and included in the analysis.Patients at the age between 61 and 80 years showed the highest incidences (n=7).ADRs of ixazommib frequently occurred within 6 weeks after the medication (n=8).Main clinical manifestations were disorders of skin,appendages (n=5),and disorders of hematologic (n=2).Moreover,there were new serious adverse reactions,for example,thrombotic microangiopathies (TMA),progressive multifocal leukoencephalopathy (PML),acute pancreaoitis (AP),and cardiotoxicity. Conclusion Physicians and pharmacists should pay more attention to the safety monitoring of ixazommib during the medication,especially for the new serious adverse reactions,and carefully assess the risk of treatment of re-administration in order for the safe and effective medication.
Key words:
Ixazommib
;
Adverse drug reactions
;
Literature analysis
开放科学(资源服务)标识码(OSID)
伊沙佐米(ixazommib)作为首个口服蛋白酶抑制剂(proteasome inhibitor,PI),与来那度胺、地塞米松联合用于治疗复发/难治多发性骨髓瘤(multiple myeloma,MM)。2015年11月获美国食品药品管理局(FDA)批准上市,2018年4月在我国上市。伊沙佐米说明书中记载的常见不良反应(adverse drug reactions,ADRs)(≥20%)有皮疹、腹泻、便秘、血小板减少、周围神经病变等[1]。目前国内尚无关于伊沙佐米致ADRs的个案报告,但国外陆续有关其导致ADRs的个案报告。本研究以国外个案报道的文献为基础,分析伊沙佐米ADRs的发生特点,以期为临床合理用药提供参考。
1 资料与方法
1.1 资料来源
检索中国知网(CNKI)、维普中文科技期刊数据库(VIP)、Pubmed数据库、Medline数据库、Web of Science数据库,中文以“伊沙佐米”、“不良反应”;英文以“ixazomib”、“Ninlaro”、“adverse”等为检索词,检索时间为2015年11月至2020年1月,收集国内外公开发表在医学期刊上关于伊沙佐米的ADRs个案报告,逐篇查阅原文,排除综述、剔除描述不详细和重复报告、以及按照《药品反应报告和监测管理办法》无法判断药品不良反应关联性的报告,得到符合条件的文献9篇[2,3,4,5,6,7,8,9,10],均为英文文献,共计10例。
BONNETA,MOREAUP.Safety of ixazomib for the treatment of multiple myeloma[J].Expert Opin Drug Saf,2017,16(8):973-980.
INTRODUCTION: Despite a major positive impact of proteasome inhibitors (PI), such as bortezomib and carfilzomib, on the survival of patients with multiple myeloma (MM) over the last few years, their use in clinical practice is limited by the development of drug resistance, significant side-effects or constraining administration schedules. Ixazomib is the first, and for now the only, oral PI, which was approved by the US Food and Drug Administration in 2015 and by the European Medicines Agency in 2016. Areas covered: In this review, we provide an overview of the preclinical and early-phase studies of ixazomib used as single-agent and in combination. Furthermore, we discuss the results of a recently published pivotal trial, which evaluated the safety profile and clinical benefit of the combination of ixazomib, lenalidomide and dexamethasone versus lenalidomide and dexamethasone alone in 722 patients with relapsed/refractory MM. Expert opinion: Ixazomib combines the comfort of oral administration, substantial clinical efficacy and a good safety profile with manageable side-effects, which mainly comprise low-grade hematological, digestive or cutaneous events, and the agent will therefore play an active part in long-term treatment strategies, both as single agent and as part of combination regimens. Ongoing phase III trials are currently defining its place in first-line, maintenance and relapse settings.
KATZH,SHENOUDAM,DAHSHAND,et al.A rare case of ixazomib-induced cutaneous necrotizing vasculitis in a patient with relapsed myeloma[J].Case Rep Hematol,2019,2019:6061484.
Ixazomib is the only oral proteasome inhibitor used in relapsed/refractory myeloma. Cutaneous side effects due to ixazomib have been documented in the literature; however, cutaneous necrotizing vasculitis is extremely rare. We describe a case of a 74-year-old man with relapsed multiple myeloma who was started on ixazomib, lenalidomide, and dexamethasone. He developed several skin lesions that were biopsied and revealed cutaneous necrotizing vasculitis. Ixazomib was held with resolution of the vasculitic lesions and restarted with dexamethasone to 20 mg on the day of treatment and 20 mg dose the day after treatment.
ALLOOA,KHOSRAVIH,GRANTER SR,et al.Ixazomib-induced cutaneous necrotizing vasculitis[J].Support Care Cancer,2018,26(7):2247-2250.
Ixazomib is a second-generation proteasome inhibitor that has been approved in the combination treatment of multiple myeloma and is currently under clinical investigation for the management of Waldenstrom's macroglobulinemia. While cutaneous adverse events secondary to proteasome inhibitors have been reported, the side effect profile of ixazomib remains to be documented. We report two patients, one with multiple myeloma and one with Waldenstrom's macroglobulinemia, who developed cutaneous necrotizing vasculitis after the initiation of ixazomib. Both patients exhibited no signs of systemic vasculitis and completed their anti-cancer regimens with resolution of their respective eruptions following dose reductions in ixazomib and initiation of low-dose prednisone. A collaborative effort towards the characterization of such cutaneous toxicities facilitates early intervention, maintenance of life-preserving anti-cancer therapy, and allows clinicians opportunity to better understand the pathophysiology of vasculitis. Moreover, appropriate identification and characterization of cutaneous toxicities from novel therapies allows providers to accurately identify safety concerns, treat toxicity, and improve patient quality of life.
ALBERTAYS,HAN SM.Drug-induced thrombotic microangiopathy due to cumulative toxicity of ixazomib[J].Case Rep Hematol,2018,2018:7063145.
Drug-induced thrombotic microangiopathies (DTMAs) are increasingly being recognized as an important category of thrombotic microangiopathies (TMAs). Cancer therapeutic agents including proteasome inhibitors (PIs) are among the most common medications reported to cause DTMA. PIs could cause DTMA either by an immune mechanism or dose-dependent/cumulative toxicity. Eleven cases of DTMA have been reported with bortezomib and carfilzomib. To the best of our knowledge, only one case of DTMA has been reported with ixazomib due to an immune-mediated mechanism. Here, we report the first case of ixazomib-induced DTMA due to cumulative toxicity rather than immune-mediated mechanism. In this article, we discuss the precipitating factors for cumulative toxicity of ixazomib, resulting in DTMA, diagnostic workup, and management of DTMA. We also discuss clinical reasoning based analysis of DTMA versus cancer-associated TMA as well as DTMA versus cyclic thrombocytopenia seen in PI use.
Progressive multifocal leukoencephalopathy (pml) is a rare demyelinating disease of the central nervous system that most often affects immunocompromised individuals. It is caused by the reactivation of the John Cunningham virus (jcv), which is found in latent form in the majority of adults. We describe a 59-year-old man with multiple myeloma who developed severe neurological deficits during treatment with ixazomib-based chemotherapy. A diagnosis of pml was established with gadolinium-enhanced magnetic resonance imaging (mri) and by detection of jcv in the cerebrospinal fluid. Despite cessation of chemotherapy and treatment with mirtazapine, he had an inexorable neurological decline and died two months after presenting to hospital. Multiple myeloma and its treatments can predispose patients to opportunistic infections including pml. Although there have been case reports of pml in patients with multiple myeloma treated with bortezomib (a different proteosome inhibitor), this is, to our knowledge, the first documented case of pml in a patient treated with a regimen that includes ixazomib.
STEINER RE,ORLOWSKI RZ,LEE HC.Acute pancreatitis associated with ixazomib in a multiple myeloma patient[J].Acta Haematol,2018,139(1):67-70.
BACKGROUND: Acute pancreatitis is an uncommon complication of anti-myeloma agents. Ixazomib is a first-in-class oral proteasome inhibitor to receive regulatory approval for the treatment of multiple myeloma. This case report describes the first case of ixazomib-associated pancreatitis. CASE PRESENTATION: An 80-year-old female with relapsed multiple myeloma presented with severe diarrhea, nausea, vomiting, abdominal pain, and acute renal failure 3 weeks after starting ixazomib and dexamethasone for disease progression. An extensive workup revealed acute pancreatitis without a definitive cause. Her condition improved with supportive measures and the discontinutation of ixazomib. The latter was suspected as the probable etiology of the patient's acute pancreatitis, given no clear alternative causes and the temporal relationship between initiating ixazomib and the development of her symptoms. CONCLUSIONS: Practitioners should include acute pancreatitis as part of their differential diagnosis in patients on ixazomib treatment who present with gastrointestinal symptoms.
GUPTAN,HANLEY MJ,XIAC,et al.Clinical pharmacology of ixazomib:the first oral proteasome inhibitor[J].Clin Pharmacokinet,2019,58(4):431-449.
Ixazomib, the first oral proteasome inhibitor, is approved in combination with lenalidomide and dexamethasone for the treatment of patients with multiple myeloma (MM) who have received at least one prior therapy. Ixazomib is a selective, potent, and reversible inhibitor of the 20S proteasome, and preferentially binds to and inhibits the beta5 chymotrypsin-like proteolytic site. Ixazomib absorption is rapid, with a median time to reach maximum plasma concentration of approximately 1 h post-dose. Ixazomib pharmacokinetics (PK) are adequately described by a three-compartment model (terminal half-life of 9.5 days) with first-order linear absorption (oral bioavailability of 58%). Plasma exposures of ixazomib increase in a dose-proportional manner. A high-fat meal decreases both the rate and extent of ixazomib absorption, supporting administration on an empty stomach. Population PK analyses demonstrated that no dose adjustment is required based on age, body size/weight, race, sex, mild-to-moderate renal impairment, or mild hepatic impairment. Results from dedicated studies indicate that a reduced starting dose (from 4 to 3 mg) is appropriate for patients with severe renal impairment, end-stage renal disease requiring dialysis, or moderate-to-severe hepatic impairment. Non-cytochrome P450 (CYP)-mediated metabolism appears to be the major clearance mechanism for ixazomib. Drug-drug interaction studies have shown no meaningful effects of strong inhibitors of CYP3A on ixazomib PK; however, the strong inducer rifampin caused a clinically relevant reduction in ixazomib exposure, supporting the recommendation to avoid concomitant administration of ixazomib with strong CYP3A inducers. Exposure-response analyses of data from the phase III TOURMALINE-MM1 registrational study demonstrate a favorable benefit-risk profile for the approved dose and regimen of weekly ixazomib 4 mg on days 1, 8, and 15 of each 28-day cycle.
CASARIN COSTA JR,VIRGENS AR,DE OLIVEIRA MESTREL,et al.Sweet syndrome:clinical features,histopathology,and associations of 83 cases[J].J Cutan Med Surg,2017,21(3):211-216.
BACKGROUND: Sweet syndrome (SS) is an infrequent skin disease characterised by sudden onset of fever, leukocytosis, neutrophilia, and tender erythematous plaques infiltrated by neutrophils. Multiple conditions have been associated with this syndrome. OBJECTIVES: The aim of this study was to evaluate the clinical, epidemiological, laboratory, and histopathological findings and associations of patients with SS. METHODS: We conducted a retrospective study of 83 patients with SS followed between January 1, 2006, and January 31, 2015. RESULTS: Of the patients, 82% were female; the mean age at onset was 48 years. Clinical presentation was mainly characterised by erythematous and edematous plaques, mostly on upper extremities and trunk. Fever was observed in 32%; 60% presented leukocytosis and 39% neutrophilia. On histopathological examination, neutrophilic and lymphohistiocytic infiltrate and edema were the most frequent findings. Fourteen percent of patients had malignancy or hematologic disorders, 26% were classified as having drug-induced SS, and 24% noted recent infection. Only 2 cases occurred during pregnancy. Systemic corticosteroid was the most common choice of treatment, with excellent response. In malignancy-associated SS, the mean hemoglobin level was lower ( P = .01) and the erythrocyte sedimentation rate (ESR) was higher ( P = .04) in comparison to classic and drug-induced SS. Leukocytoclasia was associated with higher risk of recurrence ( P = .01). CONCLUSION: All patients with SS deserve careful investigation of possible underlying conditions. Higher ESR and lower hemoglobin levels might reinforce the need of malignancy screening. Also, leukocytoclasia appears to be a potential marker of higher recurrence rate, demanding closer and longer follow-up.
REESE JA,BOUGIE DW,CURTIS BR,et al.Drug-induced thrombotic microangiopathy:experience of the oklahoma registry and the blood center of Wisconsin[J].Am J Hematol,2015,90(5):406-410.
Many drugs have been reported to cause thrombotic microangiopathy (TMA), often described as thrombotic thrombocytopenic purpura (TTP) or hemolytic-uremic syndrome (HUS). We recently established criteria to evaluate the evidence for a causal association of a drug with TMA and then we systematically reviewed all published reports of drug-induced TMA (DITMA) to determine the level of evidence supporting a causal association of the suspected drug with TMA. On the basis of this experience, we used these evaluation criteria to assess the Oklahoma TTP-HUS Registry patients who had been previously categorized as drug-induced, 1989-2014. We also reviewed the experience of the BloodCenter of Wisconsin with testing for drug-dependent antibodies reactive with platelets and neutrophils in patients with suspected immune-mediated DITMA, 1988-2014. Among 58 patients in the Oklahoma Registry previously categorized as drug-induced (15 suspected drugs), 21 patients (three drugs: gemcitabine, pentostatin, quinine) had evidence supporting a definite association with TMA; 19 (90%) of the 21 patients had quinine-induced TMA. The BloodCenter of Wisconsin tested 40 patients with suspected DITMA (eight drugs); drug-dependent antibodies, supporting a definite association with TMA, were identified in 30 patients (three drugs: oxaliplatin, quinine, vancomycin); 28 (93%) of the 30 patients had quinine-induced TMA. Combining the data from these two sources, 51 patients (five drugs) have been identified with evidence supporting a definite association with TMA. DITMA was attributed to quinine in 47 (92%) of these 51 patients.
LONIALS,WALLER EK,RICHARDSON PG,et al.Risk factors and kinetics of thrombocytopenia associated with bortezomib for relapsed,refractory multiple myeloma[J].Blood,2005,106(12):3777-3784.
Bortezomib, a proteasome inhibitor with efficacy in multiple myeloma, is associated with thrombocytopenia, the cause and kinetics of which are different from those of standard cytotoxic agents. We assessed the frequency, kinetics, and mechanism of thrombocytopenia following treatment with bortezomib 1.3 mg/m2 in 228 patients with relapsed and/or refractory myeloma in 2 phase 2 trials. The mean platelet count decreased by approximately 60% during treatment but recovered rapidly between treatments in a cyclic fashion. Among responders, the pretreatment platelet count increased significantly during subsequent cycles of therapy. The mean percent reduction in platelets was independent of baseline platelet count, M-protein concentration, and marrow plasmacytosis. Plasma thrombopoietin levels inversely correlated with platelet count. Murine studies demonstrated a reduction in peripheral platelet count following a single bortezomib dose without negative effects on megakaryocytic cellularity, ploidy, or morphology. These data suggest that bortezomib-induced thrombocytopenia is due to a reversible effect on megakaryocytic function rather than a direct cytotoxic effect on megakaryocytes or their progenitors. The exact mechanism underlying bortezomib-induced thrombocytopenia remains unknown but it is unlikely to be related to marrow injury or decreased thrombopoietin production.
SHATZEL JJ,TAYLOR JA.Syndromes of thrombotic microangiopathy[J].Med Clin North Am,2017,101(2):395-415.
Thrombotic thrombocytopenia purpura (TTP) and the hemolytic uremic syndrome (HUS) are rare thrombotic microangiopathies that can be rapidly fatal. Although the acquired versions of TTP and HUS are generally highest on this broad differential, multiple rarer entities can produce a clinical picture similar to TTP/HUS, including microangiopathic hemolysis, renal failure, and neurologic compromise. More recent analysis has discovered a host of genetic factors that can produce microangiopathic hemolytic syndromes. This article discusses the current understanding of thrombotic microangiopathy and outlines the pathophysiology and causative agents associated with each distinct syndrome as well as the most accepted treatments.
VERMERSCHP,KAPPOSL,GOLDR,et al.Clinical outcomes of natalizumab-associated progressive multifocal leukoencephalopathy[J].Neurology,2011,76(20):1697-1704.
OBJECTIVE: Natalizumab, a therapy for multiple sclerosis (MS), has been associated with progressive multifocal leukoencephalopathy (PML), a rare opportunistic infection of the CNS associated with the JC virus. We assessed clinical outcomes and identified variables associated with survival in 35 patients with natalizumab-associated PML. METHODS: Physicians provided Karnofsky scores and narrative descriptions of clinical status. Data were supplemented by the natalizumab global safety database. RESULTS: At the time of analysis, 25 patients (71%) had survived. Survivors were younger (median 40 vs 54 years) and had lower pre-PML Expanded Disability Status Scale scores (median 3.5 vs 5.5) and a shorter time from symptom onset to diagnosis (mean 44 vs 63 days) compared with individuals with fatal cases. Of patients with nonfatal cases, 86% had unilobar or multilobar disease on brain MRI at diagnosis, whereas 70% of those with fatal cases had widespread disease. Gender, MS duration, natalizumab exposure, prior immunosuppressant use, and CSF JC viral load at diagnosis were comparable. Most patients were treated with rapid removal of natalizumab from the circulation. The majority of patients developed immune reconstitution inflammatory syndrome and were treated with corticosteroids. Among survivors with at least 6 months follow-up, disability levels were evenly distributed among mild, moderate, and severe, based on physician-reported Karnofsky scores. CONCLUSIONS: Natalizumab-associated PML has improved survival compared with PML in other populations. Disability in survivors ranged from mild to severe. A shorter time from symptom onset to diagnosis and localized disease on MRI at diagnosis were associated with improved survival. These data suggest that earlier diagnosis through enhanced clinical vigilance and aggressive management may improve outcomes.
TALAMOG,SIVIKJ,PANDEY MK,et al.Bortezomib-induced acute pancreatitis:case report and review of the literature[J].J Oncol Pharm Pract,2016,22(2):332-334.
Acute pancreatitis is a rare complication of chemotherapy agents. We describe the case of a patient with multiple myeloma who developed acute pancreatitis after treatment with bortezomib, a proteasome inhibitor commonly used in the treatment of this disease. We reviewed the available medical literature on this topic, and found other seven similar cases, all after intravenous bortezomib. Our case is the first one occurring with the subcutaneous route of administration.
KONG XT,NGUYEN NT,CHOI YJ,et al.Phase 2 Study of bortezomib combined with temozolomide and regional radiation therapy for upfront treatment of patients with newly diagnosed glioblastoma multiforme:safety and efficacy assessment[J].Int J Radiat Oncol Biol Phys,2018,100(5):1195-1203.
PURPOSE: To assess the safety and efficacy of upfront treatment using bortezomib combined with standard radiation therapy (RT) and temozolomide (TMZ), followed by adjuvant bortezomib and TMZ for /=18 months compared with historical norms (25.0% at 18 and 24 months; 16.7% at 30 months). In terms of overall survival (OS), the median OS was 19.1 months (95% CI 6.7-31.4), with improved OS rates at >/=12 months (87.5% at 12, 50.0% at 24, 34.1% at 36-60 months) compared with the historical norms. The median PFS was 24.7 months (95% CI 8.5-41.0) in 10 MGMT methylated and 5.1 months (95% CI 3.9-6.2) in 13 unmethylated patients. The estimated median OS was 61 months (95% CI upper bound not reached) in the methylated and 16.4 months (95% CI 11.8-21.0) in the unmethylated patients. CONCLUSIONS: The addition of bortezomib to current standard radiochemotherapy in newly diagnosed GBM patients was tolerable. The PFS and OS rates appeared promising, with more benefit to MGMT methylated patients. Further clinical investigation is warranted in a larger cohort of patients.
The proteasome prevents the intracellular accumulation of proteins and its impairment can lead to structural and functional alterations, as noted for the coronary vasculature in a previous study. Utilizing the same model, this study was designed to test the hypothesis that chronic proteasome inhibition (PSI) also leads to structural and functional changes of the heart. Female domestic pigs were randomized to a normal diet without (N) or with twice-weekly subcutaneous injections of the proteasome inhibitor MLN-273 (0.08 mg/kg, N PSI, n 5 each group). In vivo data on cardiac structure and function as well as myocardial perfusion and microvascular permeability response to adenosine and dobutamine were obtained by electron beam computed tomography after 11 weeks. Subsequent ex vivo myocardial analyses included immunoblotting, immunostaining, TUNEL (terminal deoxynucleotidyl transferase dUTP nick end labelling), Masson trichrome, and Congo red staining. Compared with N, an increase in LV mass was observed in N PSI (106.5 16.4 g vs. 183.1 24.2 g, P 0.05). The early to late diastolic filling ratio was increased in N PSI vs. N (3.5 0.6 vs. 1.8 0.1, P 0.05). The EF tended to be lower (46 12 and 53 9, respectively) and cardiac output was significantly lower in N PSI than in N (2.9 1.1 vs. 4.7 1.1 L/min, P 0.05). Tissue analyses demonstrated an accumulation of proteasome substrates, apoptosis, and fibrosis in the PSI group. Compared with N, the myocardial perfusion response was reduced and microvascular permeability was increased in N PSI. The current study demonstrates that chronic proeasome inhibition affects the cardiovascular system, leading to functional and structural alteration of the heart consistent with a hypertrophicrestrictive cardiomyopathy phenotype.
Safety of ixazomib for the treatment of multiple myeloma
1
2017
... 伊沙佐米(ixazommib)作为首个口服蛋白酶抑制剂(proteasome inhibitor,PI),与来那度胺、地塞米松联合用于治疗复发/难治多发性骨髓瘤(multiple myeloma,MM).2015年11月获美国食品药品管理局(FDA)批准上市,2018年4月在我国上市.伊沙佐米说明书中记载的常见不良反应(adverse drug reactions,ADRs)(≥20%)有皮疹、腹泻、便秘、血小板减少、周围神经病变等[1].目前国内尚无关于伊沙佐米致ADRs的个案报告,但国外陆续有关其导致ADRs的个案报告.本研究以国外个案报道的文献为基础,分析伊沙佐米ADRs的发生特点,以期为临床合理用药提供参考. ...
Ixazomib-induced Sweet's syndrome
1
2020
... 检索中国知网(CNKI)、维普中文科技期刊数据库(VIP)、Pubmed数据库、Medline数据库、Web of Science数据库,中文以“伊沙佐米”、“不良反应”;英文以“ixazomib”、“Ninlaro”、“adverse”等为检索词,检索时间为2015年11月至2020年1月,收集国内外公开发表在医学期刊上关于伊沙佐米的ADRs个案报告,逐篇查阅原文,排除综述、剔除描述不详细和重复报告、以及按照《药品反应报告和监测管理办法》无法判断药品不良反应关联性的报告,得到符合条件的文献9篇[2,3,4,5,6,7,8,9,10],均为英文文献,共计10例. ...
Ixazomib-induced Sweet's syndrome
1
2019
... 检索中国知网(CNKI)、维普中文科技期刊数据库(VIP)、Pubmed数据库、Medline数据库、Web of Science数据库,中文以“伊沙佐米”、“不良反应”;英文以“ixazomib”、“Ninlaro”、“adverse”等为检索词,检索时间为2015年11月至2020年1月,收集国内外公开发表在医学期刊上关于伊沙佐米的ADRs个案报告,逐篇查阅原文,排除综述、剔除描述不详细和重复报告、以及按照《药品反应报告和监测管理办法》无法判断药品不良反应关联性的报告,得到符合条件的文献9篇[2,3,4,5,6,7,8,9,10],均为英文文献,共计10例. ...
A rare case of ixazomib-induced cutaneous necrotizing vasculitis in a patient with relapsed myeloma
1
2019
... 检索中国知网(CNKI)、维普中文科技期刊数据库(VIP)、Pubmed数据库、Medline数据库、Web of Science数据库,中文以“伊沙佐米”、“不良反应”;英文以“ixazomib”、“Ninlaro”、“adverse”等为检索词,检索时间为2015年11月至2020年1月,收集国内外公开发表在医学期刊上关于伊沙佐米的ADRs个案报告,逐篇查阅原文,排除综述、剔除描述不详细和重复报告、以及按照《药品反应报告和监测管理办法》无法判断药品不良反应关联性的报告,得到符合条件的文献9篇[2,3,4,5,6,7,8,9,10],均为英文文献,共计10例. ...
Ixazomib-induced cutaneous necrotizing vasculitis
1
2018
... 检索中国知网(CNKI)、维普中文科技期刊数据库(VIP)、Pubmed数据库、Medline数据库、Web of Science数据库,中文以“伊沙佐米”、“不良反应”;英文以“ixazomib”、“Ninlaro”、“adverse”等为检索词,检索时间为2015年11月至2020年1月,收集国内外公开发表在医学期刊上关于伊沙佐米的ADRs个案报告,逐篇查阅原文,排除综述、剔除描述不详细和重复报告、以及按照《药品反应报告和监测管理办法》无法判断药品不良反应关联性的报告,得到符合条件的文献9篇[2,3,4,5,6,7,8,9,10],均为英文文献,共计10例. ...
Ixazomib-induced thrombotic microangiopathy
2
2017
... 检索中国知网(CNKI)、维普中文科技期刊数据库(VIP)、Pubmed数据库、Medline数据库、Web of Science数据库,中文以“伊沙佐米”、“不良反应”;英文以“ixazomib”、“Ninlaro”、“adverse”等为检索词,检索时间为2015年11月至2020年1月,收集国内外公开发表在医学期刊上关于伊沙佐米的ADRs个案报告,逐篇查阅原文,排除综述、剔除描述不详细和重复报告、以及按照《药品反应报告和监测管理办法》无法判断药品不良反应关联性的报告,得到符合条件的文献9篇[2,3,4,5,6,7,8,9,10],均为英文文献,共计10例. ...
Drug-induced thrombotic microangiopathy due to cumulative toxicity of ixazomib
1
2018
... 检索中国知网(CNKI)、维普中文科技期刊数据库(VIP)、Pubmed数据库、Medline数据库、Web of Science数据库,中文以“伊沙佐米”、“不良反应”;英文以“ixazomib”、“Ninlaro”、“adverse”等为检索词,检索时间为2015年11月至2020年1月,收集国内外公开发表在医学期刊上关于伊沙佐米的ADRs个案报告,逐篇查阅原文,排除综述、剔除描述不详细和重复报告、以及按照《药品反应报告和监测管理办法》无法判断药品不良反应关联性的报告,得到符合条件的文献9篇[2,3,4,5,6,7,8,9,10],均为英文文献,共计10例. ...
Progressive multifocal leukoencephalopathy during ixazomib-based chemotherapy
1
2018
... 检索中国知网(CNKI)、维普中文科技期刊数据库(VIP)、Pubmed数据库、Medline数据库、Web of Science数据库,中文以“伊沙佐米”、“不良反应”;英文以“ixazomib”、“Ninlaro”、“adverse”等为检索词,检索时间为2015年11月至2020年1月,收集国内外公开发表在医学期刊上关于伊沙佐米的ADRs个案报告,逐篇查阅原文,排除综述、剔除描述不详细和重复报告、以及按照《药品反应报告和监测管理办法》无法判断药品不良反应关联性的报告,得到符合条件的文献9篇[2,3,4,5,6,7,8,9,10],均为英文文献,共计10例. ...
Acute pancreatitis associated with ixazomib in a multiple myeloma patient
1
2018
... 检索中国知网(CNKI)、维普中文科技期刊数据库(VIP)、Pubmed数据库、Medline数据库、Web of Science数据库,中文以“伊沙佐米”、“不良反应”;英文以“ixazomib”、“Ninlaro”、“adverse”等为检索词,检索时间为2015年11月至2020年1月,收集国内外公开发表在医学期刊上关于伊沙佐米的ADRs个案报告,逐篇查阅原文,排除综述、剔除描述不详细和重复报告、以及按照《药品反应报告和监测管理办法》无法判断药品不良反应关联性的报告,得到符合条件的文献9篇[2,3,4,5,6,7,8,9,10],均为英文文献,共计10例. ...
Ixazomib cardiotoxicity:a possible class effect of proteasome inhibitors
1
2017
... 检索中国知网(CNKI)、维普中文科技期刊数据库(VIP)、Pubmed数据库、Medline数据库、Web of Science数据库,中文以“伊沙佐米”、“不良反应”;英文以“ixazomib”、“Ninlaro”、“adverse”等为检索词,检索时间为2015年11月至2020年1月,收集国内外公开发表在医学期刊上关于伊沙佐米的ADRs个案报告,逐篇查阅原文,排除综述、剔除描述不详细和重复报告、以及按照《药品反应报告和监测管理办法》无法判断药品不良反应关联性的报告,得到符合条件的文献9篇[2,3,4,5,6,7,8,9,10],均为英文文献,共计10例. ...
Clinical pharmacology of ixazomib:the first oral proteasome inhibitor
Phase 2 Study of bortezomib combined with temozolomide and regional radiation therapy for upfront treatment of patients with newly diagnosed glioblastoma multiforme:safety and efficacy assessment
, 方玉婷, 李民
