Acute Pancreatitis Associated with Ixazomib in a Multiple Myeloma Patient

2018 ◽  
Vol 139 (1) ◽  
pp. 67-70 ◽  
Author(s):  
Raphael E. Steiner ◽  
Robert Z. Orlowski ◽  
Hans C. Lee
Keyword(s):  
Multiple Myeloma ◽  
Acute Pancreatitis ◽  
Proteasome Inhibitor ◽  
Gastrointestinal Symptoms ◽  
Multiple Myeloma Patient ◽  
Case Presentation ◽  
Severe Diarrhea ◽  
First Case ◽  
To Receive ◽  
Uncommon Complication

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.

scholarly journals Bortezomib-Induced Perimyocarditis in a Multiple Myeloma Patient: A Case Report

2021 ◽  
pp. 1853-1859
Author(s):  
Yaman Alali ◽  
Muhamed Baljevic
Keyword(s):  
Multiple Myeloma ◽  
Pericardial Effusion ◽  
Proteasome Inhibitor ◽  
Troponin I ◽  
Acute Myocarditis ◽  
Cardiovascular Complications ◽  
Pleuritic Chest Pain ◽  
Multiple Myeloma Patient ◽  
First Case ◽  
Scoring Tools

Bortezomib (BTZ) is a proteasome inhibitor used in the treatment of multiple myeloma (MM) and other hematological malignancies. Although carfilzomib, a second-generation proteasome inhibitor, is most strongly associated with cardiotoxicity, BTZ has been associated with several cardiovascular complications including congestive heart failure, arrhythmias, and rarely myocarditis. Here, we report the first case of a BTZ-induced perimyocarditis. The patient was a 40-year-old woman with recently diagnosed MM who was admitted to the hospital with syncope at the start of her second cycle of induction therapy with BTZ, lenalidomide, and dexamethasone. She had a witnessed syncopal event in the emergency room with the telemetry showing sustained ventricular tachycardia. Laboratory workup showed elevated N-terminal pro B-type natriuretic peptide and normal troponin I. Transthoracic echocardiogram (TTE) showed a low ejection fraction of 40% with global hypokinesis of the left ventricle and trace pericardial effusion. Cardiac magnetic resonance imaging with gadolinium was consistent with acute myocarditis. The patient had recurrent pleuritic chest pain, and a repeat TTE showed worsening pericardial effusion consistent with pericarditis. Endomyocardial biopsy was done which showed nonspecific myocyte hypertrophy and foci of fibrosis, but was negative for giant cell myocarditis, hemochromatosis, and amyloidosis. Extensive infectious disease workup ruled out known infectious causes for perimyocarditis. Given the close timing between BTZ treatment (5 subcutaneous doses with a cumulative dose of 6.5 mg/m<sup>2</sup>), the absence of other iatrogenic or infectious causes, and probable or likely association with BTZ as assessed by the validated causality assessment scoring tools, it was concluded that the acute perimyocarditis was secondary to BTZ exposure. Here, we report the first case of BTZ-induced perimyocarditis and discuss the incidence and pathophysiology of BTZ-cardiovascular toxicity.

scholarly journals Acute Liver Rejection in a Multiple Myeloma Patient Treated with Lenalidomide

2020 ◽  
Vol 2020 ◽  
pp. 1-4
Author(s):  
Iuliana Vaxman ◽  
John Eaton ◽  
Hee Eun Lee ◽  
Morie A. Gertz
Keyword(s):  
Multiple Myeloma ◽  
Mycophenolate Mofetil ◽  
Case Report ◽  
Allograft Rejection ◽  
Acute Cellular Rejection ◽  
Primary Biliary Cholangitis ◽  
Myeloma Patient ◽  
Multiple Myeloma Patient ◽  
First Case ◽  
Cellular Rejection

Herein we present a patient that underwent a liver transplant due to primary biliary cholangitis (PBC) and after 9 years developed multiple myeloma. Following the cessation of mycophenolate mofetil and 2 weeks after lenalidomide treatment was started, the patient experienced acute cellular rejection. The patient recovered after treatment with corticosteroids, resumption of mycophenolate mofetil, and cessation of lenalidomide. Lenalidomide-associated allograft rejection has been reported in other organs. However, this is the first case report of liver rejection induced by lenalidomide.

Impact of proteasome inhibitor vs. IMiD maintenance therapy on outcomes of patients with high-risk multiple myeloma (HRMM).

2020 ◽  
Vol 38 (15_suppl) ◽  
pp. e20557-e20557
Author(s):  
Eric Leon Tam ◽  
David Joseph Iberri ◽  
Michaela Liedtke ◽  
Lori S. Muffly ◽  
Parveen Shiraz ◽  
...  
Keyword(s):  
Multiple Myeloma ◽  
High Risk ◽  
Maintenance Therapy ◽  
Proteasome Inhibitor ◽  
Post Transplant ◽  
Risk Patients ◽  
To Receive ◽  
Standard Risk

e20557 Background: The ideal choice of maintenance therapy in patients with HRMM high-risk multiple myeloma remains unknown. We analyzed the outcomes of patients with HRMM undergoing transplant receiving different maintenance approaches. Methods: Patients with MM undergoing their first ASCT from 2012-19 within 1 year of diagnosis were identified from the prospectively maintained database of patients undergoing ASCT. HRMM was defined as having t(4;14), t(14;16), t(14;20), del17p13, or gain 1q detected on fluorescent in situ hybridization (FISH). Results: Of the 412 patients undergoing ASCT within 1 year of diagnosis, 333 had FISH data available and of these, 37% (124/333) patients had high-risk cytogenetics. Distribution of HR cytogenetics was as follows: deletion 17p: 37% (n = 46), t(4;14): 27% (n = 34), t(14;16) or t(14;20): 12% (n = 26), gain1q: 31% (n = 41). 9% (n = 12) had more than one HR abnormality. In patients with HRMM, median age at transplant was 59 years (range: 39 to 73), and 61% (n = 103) were males. 64% (n = 107) of high-risk patients received post-transplant maintenance therapy. Maintenance therapy in this group included a proteasome inhibitor (PI) in 34% (n = 29), immunomodulatory drug (IMiD) in 59% (n = 51), or both in 7% (n = 6). There was no difference in baseline characteristics of HRMM patients receiving PI vs. IMiD maintenance, except that patients with del17p were more likely to receive PI maintenance therapy (55% vs 28%, p = 0.01). (Table) After a median follow-up of 3.1 years from diagnosis, patients with HRMM had inferior PFS compared to patients with standard risk disease, with median PFS of 3 vs. 4.8 years, p < 0.001. Amongst the 86 HRMM patients receiving maintenance therapy, median PFS in patients receiving PI vs. IMiD vs. both PI + IMiD maintenance was 3 vs. 3.2 vs. 2.2 years, respectively, log-rank p = 0.7. In the sub-group of patients with 17p deletion, median PFS in the three groups was 3 vs. 2.9 vs. 2.2 years, respectively, log-rank p = 0.7. Conclusions: Patients with HRMM have inferior PFS compared to patients with standard risk disease. We observed similar outcomes in HRMM patients post-transplant regardless of the choice of maintenance therapy. [Table: see text]

Duodeno-jejunal Intussusception with Acute Pancreatitis in Peutz-Jeghers Syndrome: The First Case Presentation in Childhood

2015 ◽  
Vol 19 (10) ◽  
pp. 1922-1924 ◽  
Author(s):  
Jiro Kimura ◽  
Kiyoshi Sasaki ◽  
Takehiro Okabayashi ◽  
Yasuo Shima ◽  
Jun Iwata ◽  
...  
Keyword(s):  
Acute Pancreatitis ◽  
Case Presentation ◽  
First Case ◽  
Peutz Jeghers Syndrome

scholarly journals Carfilzomib, lenalidomide, dexamethasone, and cyclophosphamide (KRdc) as induction therapy for transplant-eligible, newly diagnosed multiple myeloma patients (Myeloma XI+): Interim analysis of an open-label randomised controlled trial

PLoS Medicine ◽  
2021 ◽  
Vol 18 (1) ◽  
pp. e1003454
Author(s):  
Graham H. Jackson ◽  
Charlotte Pawlyn ◽  
David A. Cairns ◽  
Ruth M. de Tute ◽  
Anna Hockaday ◽  
...  
Keyword(s):  
Multiple Myeloma ◽  
Partial Response ◽  
Interim Analysis ◽  
Proteasome Inhibitor ◽  
Group Versus ◽  
Control Group ◽  
Newly Diagnosed ◽  
To Receive ◽  
Good Partial Response

Background Carfilzomib is a second-generation irreversible proteasome inhibitor that is efficacious in the treatment of myeloma and carries less risk of peripheral neuropathy than first-generation proteasome inhibitors, making it more amenable to combination therapy. Methods and findings The Myeloma XI+ trial recruited patients from 88 sites across the UK between 5 December 2013 and 20 April 2016. Patients with newly diagnosed multiple myeloma eligible for transplantation were randomly assigned to receive the combination carfilzomib, lenalidomide, dexamethasone, and cyclophosphamide (KRdc) or a triplet of lenalidomide, dexamethasone, and cyclophosphamide (Rdc) or thalidomide, dexamethasone, and cyclophosphamide (Tdc). All patients were planned to receive an autologous stem cell transplantation (ASCT) prior to a randomisation between lenalidomide maintenance and observation. Eligible patients were aged over 18 years and had symptomatic myeloma. The co-primary endpoints for the study were progression-free survival (PFS) and overall survival (OS) for KRdc versus the Tdc/Rdc control group by intention to treat. PFS, response, and safety outcomes are reported following a planned interim analysis. The trial is registered (ISRCTN49407852) and has completed recruitment. In total, 1,056 patients (median age 61 years, range 33 to 75, 39.1% female) underwent induction randomisation to KRdc (n = 526) or control (Tdc/Rdc, n = 530). After a median follow-up of 34.5 months, KRdc was associated with a significantly longer PFS than the triplet control group (hazard ratio 0.63, 95% CI 0.51–0.76). The median PFS for patients receiving KRdc is not yet estimable, versus 36.2 months for the triplet control group (p < 0.001). Improved PFS was consistent across subgroups of patients including those with genetically high-risk disease. At the end of induction, the percentage of patients achieving at least a very good partial response was 82.3% in the KRdc group versus 58.9% in the control group (odds ratio 4.35, 95% CI 3.19–5.94, p < 0.001). Minimal residual disease negativity (cutoff 4 × 10−5 bone marrow leucocytes) was achieved in 55% of patients tested in the KRdc group at the end of induction, increasing to 75% of those tested after ASCT. The most common adverse events were haematological, with a low incidence of cardiac events. The trial continues to follow up patients to the co-primary endpoint of OS and for planned long-term follow-up analysis. Limitations of the study include a lack of blinding to treatment regimen and that the triplet control regimen did not include a proteasome inhibitor for all patients, which would be considered a current standard of care in many parts of the world. Conclusions The KRdc combination was well tolerated and was associated with both an increased percentage of patients achieving at least a very good partial response and a significant PFS benefit compared to immunomodulatory-agent-based triplet therapy. Trial registration ClinicalTrials.gov ISRCTN49407852.

scholarly journals A case of SFTS coinfected with E. coli bacteremia

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Hyungdon Lee ◽  
Woo Young Choi ◽  
Choon Mee Kim ◽  
Na-Ra Yun ◽  
Dong-Min Kim ◽  
...  
Keyword(s):  
Liver Function ◽  
Foley Catheter ◽  
Gastrointestinal Symptoms ◽  
Hemorrhagic Fever ◽  
Case Presentation ◽  
E Coli ◽  
First Case ◽  
Low Blood Pressure ◽  
Severe Fever ◽  
Conjunctival Hemorrhage

Abstract Background Severe fever thrombocytopenia syndrome virus (SFTSV) is the causative agent of severe fever thrombocytopenia syndrome (SFTS). SFTS is an emerging infectious disease, characterized by high fever, gastrointestinal symptoms, leukopenia, thrombocytopenia, and a high mortality rate. Until now, little importance has been given to the association of SFTS with leukocytosis and bacterial co-infection. Case presentation A 51-year old man visited our hospital with fever and low blood pressure. He was a farmer by occupation and often worked outdoors. He had a Foley catheter inserted due to severe BPH. Laboratory tests revealed thrombocytopenia, elevated liver function, and elevated CRP levels. He had marked leukocytosis, proteinuria, hematuria, and conjunctival hemorrhage. Initially, we thought that the patient was suffering from hemorrhagic fever with renal syndrome (HFRS). However, we confirmed SFTS through PCR and increasing antibody titer. However, his blood culture also indicated E. coli infection. Conclusion SFTS displays characteristics of fever, thrombocytopenia, elevated liver function, and leukocytopenia. We described a case of SFTS with leukocytosis due to coinfection with E. coli. Since patients with SFTS usually have leukocytopenia, SFTS patients with leukocytosis are necessarily evaluated for other causes of leukocytosis. Here, we report the first case of an SFTS with concurrent E. coli bacteremia.

scholarly journals Case Report of a Rare Incidence of IgH Amplification Leading to Acute Kidney Injury in a Multiple Myeloma Patient

2021 ◽  
pp. 274-278
Author(s):  
Sowmya Thanikachalam ◽  
Vijay Kumar Srinivasalu ◽  
K.S. Nataraj ◽  
Sharat Damodar ◽  
Manjula Das
Keyword(s):  
Multiple Myeloma ◽  
Acute Kidney Injury ◽  
Case Report ◽  
Heavy Chain ◽  
Kidney Injury ◽  
Bone Marrow Aspiration ◽  
Structural Abnormality ◽  
Cell Transplant ◽  
Multiple Myeloma Patient ◽  
First Case

We present a case report of a 62-year-old male, treated for kappa light chain multiple myeloma with chemotherapy followed by autologous stem cell transplant (ASCT) in 2014. He has been in complete remission for 4 years. In 2018, he was evaluated for hypercreatinemia and acute kidney injury(AKI) with a suspicion of disease relapse; he underwent evaluation with bone marrow aspiration cytology which showed no evidence of relapse. However, careful cytogenetic analyses showed IgH amplification (14q32) which probably was the cause for AKI in the absence of any structural abnormality in the kidney. Heavy chain deposition leads to AKI in multiple myeloma, and its association with IgH amplification leading to AKI is reported here. Though heavy chain deposition leading to AKI is common, IgH amplification at chromosome level is the first case observed.

Malignant Pericardial Effusion--An Uncommon Complication of Multiple Myeloma: Case Report

2005 ◽  
Vol 8 (2) ◽  
pp. 87 ◽  
Author(s):  
Louis E. Samuels ◽  
Philbert Y. Van ◽  
Douglas E Gladstone ◽  
Marian M. Haber
Keyword(s):  
Multiple Myeloma ◽  
Case Report ◽  
Plasma Cells ◽  
Pericardial Fluid ◽  
Pleural Effusions ◽  
Myeloma Patient ◽  
Multiple Myeloma Patient ◽  
Malignant Pericardial Effusion ◽  
Abnormal Accumulation ◽  
Uncommon Complication

Multiple myeloma is a condition usually associated with lesions of the skeleton. However, under rare circumstances, the malignant plasma cells may infiltrate the pericardium, resulting in an effusion. If left untreated, the abnormal accumulation of pericardial fluid will result in cardiac tamponade, requiring drainage. The following report describes a multiple myeloma patient who developed secondary pericardial and pleural effusions, which were surgically drained via a pleuropericardial window.

Bortezomib-induced motor neuropathy: A case report

2020 ◽  
Vol 26 (6) ◽  
pp. 1549-1552 ◽  
Author(s):  
Meghana Singh ◽  
Vinay M Thomas ◽  
Sudhanshu Mulay
Keyword(s):  
Risk Factors ◽  
Adverse Effect ◽  
Multiple Myeloma ◽  
Case Report ◽  
Proteasome Inhibitor ◽  
Cell Lymphoma ◽  
Gastrointestinal Symptoms ◽  
Motor Neuropathy ◽  
Lower Extremity Weakness ◽  
Mantle Cell

Introduction Bortezomib is a proteasome inhibitor used in the treatment of multiple myeloma, Waldenström’s macroglobulinemia, mantle cell lymphoma. The most reported adverse effects include fatigue, thrombocytopenia, gastrointestinal symptoms, and peripheral neuropathy, which mostly manifests as sensory neuropathic symptoms. We present a case of a patient who experienced motor neuropathy after initiating treatment with bortezomib. Case report An 87-year-old male was diagnosed with multiple myeloma and started on treatment with bortezomib, dexamethasone, and lenalidomide (VRd). After five cycles of therapy, he developed lower extremity weakness, which was severely debilitating, affecting his ability to walk, and this prompted his visit to the emergency department. Management and outcome The patient was admitted for further workup and underwent electromyography, which was consistent with demyelinating polyneuropathy with active denervation. His symptoms were attributed to bortezomib, and his VRd regimen was held. His symptoms failed to improve despite discontinuation of bortezomib. He then received steroids and intravenous immunoglobulin (IViG) with a gradual resolution of his symptoms. He was thereafter restarted on only lenalidomide and dexamethasone with no recurrence of his neuropathy. Discussion Clinicians need to be aware of the likely risk for motor neuropathy associated with bortezomib. Risk factors like older age and pre-existing neuropathy can predispose patients to this adverse effect, and clinicians should monitor for this toxicity and facilitate dose reduction or discontinuation of therapy if warranted. Sometimes, patients may also need further treatment with steroids or IVIG.

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