MO232BORTEZOMIB INDUCED PERIPHERAL AND CENTRAL NEUROPATHY : ABOUT 3 CASE REPORTS

2021 ◽  
Vol 36 (Supplement_1) ◽  
Author(s):  
Rawnak Houli ◽  
Samia Barbouche ◽  
Hajji Mariem ◽  
Amira Sakay ◽  
Samarra Badrouchi ◽  
...  
Keyword(s):  
Multiple Myeloma ◽  
Case Reports ◽  
Sensory Neuropathy ◽  
Deficiency Syndrome ◽  
Clonic Seizure ◽  
Prior History ◽  
Cerebral Mri ◽  
History Of ◽  
Balance Disorder ◽  
Peripheral Sensory

Abstract Background and Aims Bortezomib is a proteasome inhibitor, whose efficacy in the treatment of multiple myeloma has been proven over the last years. However, its side effects may cause concern for patients as well as physicians. We focused in this study on Bortezomib-induced neuropathy, one of the most frequent complications. We present 2 cases of peripheral sensory neuropathy and one intriguing case of central neurological manifestation, all caused by Bortezomib administration. Case 1 A 62-year-old man, with a history of diabetes and hypertension, was diagnosed with multiple myeloma in 2019. He received 2 cycles of Bortezamib (2,5 mg), Dexamethasone , and Cyclophosphamide. Each cycle included 4 doses of Bortezomib, and the cycles were 21 days apart. At the end of the second cycle the patient developed posterior cord syndrome with balance disorder and lower extremities paresthesia. Axonal sensitivo-motor polyneuropathy was confirmed by electromyography. A pharmacology investigation was conducted, and the symptoms were attributed to Bortezomib toxicity. Evolution was favourable after change in protocol to Revlimide. No recurrence was noted. Case 2 A 64-year-old man with no prior history was diagnosed with multiple myeloma in 2020. She received a protocol of 4 cycles, 21 days apart, of Bortezomib (2.1 mg) ,Dexamethasone and Thalidomide . Three weeks after the first cycle, the patient presented with confusion, gait disturbance and four-limb pyramidal deficiency syndrome. Electromyography showed axonal sensitivo-motor polyneuropathy .In the absence of other causes, Bortezomib toxicity was suspected and the patient underwent an emergency epurative hemodialysis session, after which symptoms completely disappeared. Bortezomib doses were then reduced. The evolution was favourable. Case 3 A 50-year-old woman was diagnosed with multiple myeloma in 2018 with Randall's disease and quadri-pyramidal syndrome. She was put on 4 courses of Bortezomib 2.4mg Cyclophosphamide and Dexamethasone, 21 days apart. After 2 coursess, she presented a generalized tonic-clonic seizure preceded by headache, dizziness and followed by speech disturbances. Biological screening for metabolic disorders and toxins was unremarkable. Cerebral MRI showed no abnormalities. Doses of Bortezomib were reduced during the following course. We then witnessed an improvement in speech and no recurrence of seizures. Conclusion Bortezomib induced neuropathy is a serious and debilitating complication to which physicians must pay special attention. This side effect can be managed by dose reduction or change of molecules. Outcomes are often favourable.

scholarly journals Clozapine-induced stuttering in the absence of known risk factors: a case report

2021 ◽  
Vol 15 (1) ◽  
Author(s):  
Florence Jaguga
Keyword(s):  
Risk Factors ◽  
Family History ◽  
Side Effect ◽  
Case Reports ◽  
Extrapyramidal Symptoms ◽  
Prior History ◽  
Case Presentation ◽  
Rare Side Effect ◽  
History Of ◽  
Electrophysiological Findings

Abstract Background Stuttering is a rare side effect of clozapine. It has been shown to occur in the presence of one or more factors such as abnormal electrophysiological findings and seizures, extrapyramidal symptoms, brain pathology, and a family history of stuttering. Few case reports have documented the occurrence of clozapine-induced stuttering in the absence of these risk factors. Case presentation A 29-year-old African male on clozapine for treatment-resistant schizophrenia presented with stuttering at a dosage of 400 mg/day that resolved with dose reduction. Electroencephalogram findings were normal, and there was no clinical evidence of seizures. The patient had no prior history or family history of stuttering, had a normal neurological examination, and showed no signs of extrapyramidal symptoms. Conclusion Clinicians ought to be aware of stuttering as a side effect of clozapine, even in the absence of known risk factors. Further research should investigate the pathophysiology of clozapine-induced stuttering.

Abstract WP190: Clinical Features of Sarcoid Patients With Ischemic Stroke

Stroke ◽  
2016 ◽  
Vol 47 (suppl_1) ◽  
Author(s):  
Ahmed Z Obeidat ◽  
Heidi Sucharew ◽  
Charles J Moomaw ◽  
Dawn O Kleindorfer ◽  
Brett M Kissela ◽  
...  
Keyword(s):  
Ischemic Stroke ◽  
Current Knowledge ◽  
Case Reports ◽  
Brain Mri ◽  
Sporadic Case ◽  
Prior History ◽  
Stroke Patients ◽  
Stroke Subtype ◽  
Stroke Event ◽  
History Of

Background: Current knowledge on ischemic stroke in sarcoid patients stems from sporadic case reports. The mechanism is thought to be related to granulomatous involvement of brain vasculature. However, clinical, demographic, and radiographic features of sarcoid patients with ischemic stroke are lacking. If sarcoid patients are at higher risk for ischemic stroke event, we hypothesized that the risk factors for ischemic stroke and stroke subtype distribution would differ between sarcoid and non-sarcoid ischemic stroke patients. Methods: Cases of ischemic stroke were identified for the years 2005 and 2010 from the population-based Greater Cincinnati/Northern Kentucky Stroke Study (population 1.3 million). Ischemic stroke cases were physician study confirmed and patients with a history of sarcoid were identified through medical chart review. Clinical variables were compared between stroke patients with history of sarcoid and those with no prior sarcoid history. Results: A total of 4258 cases of ischemic stroke were identified; of them, only 18 had prior diagnosis of sarcoid (0.04%). Brain MRI showed diffusion restriction in 14 out of 15 (93%) MRIs performed in sarcoid patients. The table presents risk factor and subtype data on sarcoid patients compared with non-sarcoid patients. Conclusions: We identified only a few cases of prior sarcoid history in our two-year ascertainment of ischemic stroke patients in our population. In comparison with stroke patients with no prior history of sarcoid, the sarcoid patients tended to be of younger age at presentation, female, have a history of diabetes and hyperlipidemia, and more likely of African descent, perhaps related to the diagnosis of sarcoid itself. We were unable to detect differences in stroke subtype distributions between sarcoid and non-sarcoid ischemic stroke patients.

scholarly journals Incidence of Second Primary Malignancies and Peripheral Sensory Neuropathy in Patients with Multiple Myeloma Receiving Daratumumab Containing Regimen

Blood ◽  
2019 ◽  
Vol 134 (Supplement_1) ◽  
pp. 5550-5550 ◽  
Author(s):  
Thura Win Htut ◽  
Donald P. Quick ◽  
Myint Aung Win ◽  
Sriman Swarup ◽  
Anita Sultan ◽  
...  
Keyword(s):  
Multiple Myeloma ◽  
Sensory Neuropathy ◽  
Phase Iii ◽  
Control Group ◽  
Second Primary ◽  
Peripheral Sensory Neuropathy ◽  
Antitumor Effects ◽  
Refractory Multiple Myeloma ◽  
Second Primary Malignancies ◽  
Peripheral Sensory

Introduction: Proteasome inhibitors-based regimens are the mainstay of initial therapy for most patients with multiple myeloma. Daratumumab is a human IgGκ monoclonal antibody that targets CD38 with direct antitumor effects and has an immunomodulatory component. Recent studies have demonstrated that addition of daratumumab to standard regimens enhance direct cytotoxicity on myeloma cells and have shown survival benefits. Yet, there are notable safety concerns. We performed a combined analysis of randomized controlled trials (RCT) to determine the risk of second primary malignancies (SPM) and peripheral sensory neuropathy (PSN) with newer daratumumab combination regimens. Methods: We systematically conducted a comprehensive literature search using MEDLINE, EMBASE databases and meeting abstracts from inception through June 2019. Phase III RCTs utilizing daratumumab in patients with multiple myeloma that mention SPM and PSN as adverse effects were incorporated in the analysis. Mantel-Haenszel (MH) method was used to calculate the estimated pooled risk ratio (RR), and risk difference (RD) with 95% confidence interval (CI). Heterogeneity was assessed with Cochran's Q- statistic. Random effects model was applied. Results: A total of 3,547 patients with multiple myeloma from 5 phase III RCTs were eligible. Studies compared daratumumab (D) + bortezomib (V) + melphan (M) + prednisone (P) vs VMP, D + lenalidomide (R) + dexamethasone (d) vs Rd, DVd vs Vd and DVd + thalidomide (T) vs VTd. The randomization ratio was 1:1 in all studies. Daratumumab was utilized in relapsed and refractory multiple myeloma in the POLLUX study (n= 564) and the CASTOR study (n= 480) and as first-line treatment for patients with multiple myeloma in the ALCYONE study (n= 700), the CASSIOPEIA study (n= 1085) and the MAIA study (n= 737). The I2 statistic for heterogeneity was 25, suggesting some heterogeneity among RCT. The SPM incidence was 76 (4.29%) in study group vs 77 (4.34%) in control group. The RR for SPM was 1.12 (95% CI: 0.74 - 1.69; P = 0.58) and RD was 0.01 (95% CI: -0.01 to 0.02; P = 0.34). The RR for SPM was noted at 2.56 (95% CI: 0.26 - 25.46; P = 0.42) in a subset of relapsed and refractory multiple myeloma. Any-grade PSN was reported in 527 (46.84%) in daratumumab arm vs 550 (48.72%) in control arm with the RR of 0.98 (95% CI: 0.80 -1.21; P = 0.88). High-grade PSN was noted in 63 (5.6%) vs 76 (6.73%) in control group with the RR of 0.73 (95% CI: 0.42 -1.27; P = 0.27). Conclusions: Our meta-analysis depicted that there was no significant increase in the risk of second primary malignancies and peripheral sensory neuropathy in patients on daratumumab combination regimen, in newly diagnosed and relapsed refractory multiple myeloma, compared to control arm. However, long-term follow-up of these patients is required to determine the actual relation with second primary malignancies. Disclosures No relevant conflicts of interest to declare.

Ki-1 Positive Anaplastic Large Cell Lymphoma Due to Immune Deficiency.

Blood ◽  
2005 ◽  
Vol 106 (11) ◽  
pp. 4709-4709
Author(s):  
Monique Chang ◽  
Jennifer Kujawa ◽  
Michael Garrison ◽  
Alexander Hindenburg
Keyword(s):  
Immune Deficiency ◽  
Anaplastic Large Cell Lymphoma ◽  
Cell Lymphoma ◽  
Case Reports ◽  
Large Cell ◽  
Hiv Positive ◽  
Prior History ◽  
Lymphoid Malignancy ◽  
History Of ◽  
Large Cell Lymphoma

Abstract Cases of Ki-1 positive anaplastic large cell lymphoma (ALCL), including ALK (t 2,5) positive and negative expression, have largely been associated with immunosuppressed transplant recipients, human immunodeficiency virus (HIV) positive patients and patients with a prior history of a lymphoproliferative disorder. We reviewed the literature and found cases of secondary Ki-1 positive ALCL in immunocompromised patients including patients with a prior history of lymphoid malignancy. Some of these latter cases may have been diagnosed initially as Hodgkin’s disease and later reclassified as Ki-1 positive ALCL. In post-transplant and HIV positive patients, severe and prolonged immunosuppression likely led to the development of Ki-1 positive ALCL. We postulate that although rare, the occurrence of Ki-1 positive ALCL in patients previously treated for a lymphoid malignancy is possible due to a pre-existing immune deficiency state. We report a case of ALK- ALCL occurring 10 years following treatment of HCL with persistent depressed T4/T8 ratio one year after achieving a complete remission of the ALCL. Secondary Cases of Ki-1 Anaplastic Large Cell Lymphoma Cases of Post-transplant Ki-1 Positive Anaplastic Large Cell Lymphoma Allograft # of Case Reports ALK (t 2,5) Renal 16 12 unknown, 4 positive Cardiac 3     1 negative, 2 positive Liver 1 1 positive Cases of Ki-1 Positive Anaplastic Large Cell Lymphoma in Patients With HIV or Treated with Immunosuppressants for Non-Malignant Disorders Cause of Immune Deficiency # of Case Reports ALK (t 2,5) HIV + 10 10 unknown Immunosuppressive tx for Evan’s syndrome 1 negative Azathioprine for Crohn’s Dz. 1 unknown Cases of Secondary Ki-1 Positive Anaplastic Large Cell Lymphoma in Patients Treated for Malignancy Primary Malignancy # of Case Reports ALK (t 2,5) Hodgkin’s Disease 3 3 unknown Hairy Cell Leukemia 2 1 unknown, 1 negative Mycosis Fungoides 2 2 unknown

B Cell Lymphoma In Association with Multiple Myeloma: Analysis of the Biologic Relationship

Blood ◽  
2011 ◽  
Vol 118 (21) ◽  
pp. 1590-1590 ◽  
Author(s):  
Anuj K. Mahindra ◽  
Aliyah R. Sohani ◽  
Christiana E. Toomey ◽  
James S. Michaelson ◽  
Jeffrey A. Barnes ◽  
...  
Keyword(s):  
Multiple Myeloma ◽  
B Cell ◽  
Board Of Directors ◽  
Light Chain ◽  
Cell Lymphoma ◽  
B Cell Lymphoma ◽  
Prior History ◽  
Advisory Committees ◽  
Age Of Diagnosis ◽  
History Of

Abstract Abstract 1590 Background: The occurrence of a secondary lymphoma in patients with a prior history of B-cell lymphomas has been reported.1, 2 There are few reported occurrences of Multiple Myeloma (MM) in patients (pts) with a prior history of lymphoma and the biologic relationship between the two neoplasms in such cases is unknown. Methods: We queried our IRB approved clinicopathologic database of hematologic malignancies for patients with lymphoma and MM. Of the 4165 pts with B-cell lymphoma and 804 pts with MM, 6 pts with a history of B-cell lymphoma developed MM and 1 patient with a prior history of MM developed a B-cell lymphoma. We describe the morphology, immunophenotype, and clinical features of the 7 pts. The clonal relationship of the 2 components was analyzed using sequencing analysis of immunoglobulin heavy chain variable region (IgVH) genes and by light chain restriction. Results: There were 5 men and 2 women (median age of diagnosis of lymphoma, 65 years; median age of diagnosis of MM, 71 years). The pts with lymphoma included 2 pts with diffuse large B cell lymphoma, 2 pts with small lymphocytic lymphoma, 2 pts with follicular lymphoma and 1 patient with lymphoplasmacytic lymphoma. The development of MM was metachronous in 5 cases, following B-cell lymphoma by 3 years to 23 years and synchronous in 1 case. In 1 patient, the B-cell lymphoma developed 6 years after the diagnosis of MM. 6 pts achieved complete remission after treatment for lymphoma and 1 patient is ongoing treatment. 6 of the 7 pts required treatment for MM soon after diagnosis. 1 patient has smoldering MM and continues to be observed 57 months after diagnosis. FISH analysis indicated IgH rearrangement in 3 pts with MM; 1 patient with 17p deletion and monosomy 13; 3 pts had normal FISH and metaphase cytogenetics. In 3 pts, both neoplasms were kappa light chain restricted; in 1 patient both were lambda restricted; in 1 patient, the lymphoma was lambda light chain restricted while the MM was kappa light chain restricted and the reverse in another pt; in 1 patient the B-cell lymphoma was light chain negative and the MM was kappa restricted. IgVH rearrangement studies in 4 patients in whom tissue samples were available indicated that the two were clonally unrelated in 3 patients and related in only 1 patient. Conclusion: Clonality analysis of rearranged immunoglobulin genes from patients with both B-cell lymphoma and MM provide evidence of separate clonal origins of the two tumors in the majority of cases, thus excluding secondary transformation of the original B-cell clone. The presence or absence of a genetic predisposition to the development of multiple B cell malignancies requires further study.3 Disclosures: Off Label Use: The combination of lenalidomide and everolimue is an off label use in multiple myeloma. Abramson:Genentech: Consultancy; Novartis: Consultancy. Raje:Amgen: Membership on an entity's Board of Directors or advisory committees; Astra Zeneca: Research Funding; Millenium: Membership on an entity's Board of Directors or advisory committees; Novartis: Membership on an entity's Board of Directors or advisory committees; Celgene: Membership on an entity's Board of Directors or advisory committees; Acetylon: Research Funding.

Multiple Myeloma Associated GI Polyposis

Blood ◽  
2012 ◽  
Vol 120 (21) ◽  
pp. 5009-5009
Author(s):  
Nassim Nabbout ◽  
Mohamad El Hawari ◽  
Thomas K. Schulz
Keyword(s):  
Multiple Myeloma ◽  
Bone Marrow ◽  
Plasma Cells ◽  
Conflicts Of Interest ◽  
Case Reports ◽  
Bone Marrow Failure ◽  
Bone Lesions ◽  
Rare Manifestation ◽  
History Of ◽  
Central Ulceration

Abstract Abstract 5009 Multiple myeloma is a neoplastic proliferation of monoclonal plasma cells that can result in osteolytic bone lesions, hypercalcemia, renal impairment, bone marrow failure, and the production of monoclonal gammopathy. The gastrointestinal tract is rarely involved in myeloma. GI polyposis is a rare manifestation of extra-medullary disease in multiple myeloma. Such cases usually present as gastrointestinal hemorrhage or intestinal obstruction. A 53-year-old African American male recently diagnosed with multiple myeloma presented with three-day history of rectal bleed and fatigue. EGD showed multiple raised, polypoid, rounded lesions with a superficial central ulceration in the stomach. Colonoscopy showed similar lesions in the ascending and transverse areas of the colon that ranged in size from 5 to 16 mm in diameter. Biopsies showed that these polyps were made of plasma cells. A bone marrow biopsy showed diffuse involvement (greater than 90%) of bone marrow with multiple myeloma with anaplastic features. The patient was started on bortezomib at diagnosis, however, he passed away a few weeks later. This type of metastatic disease has been described in isolated case reports in the literature, while solitary GI plasmacytoma has been reported more frequently. In rare cases, multiple myeloma can involve the GI tract which may lead to bleed or obstruction. This involvement is likely a marker of aggressivity. This example of extra-medullary disease in myeloma is an uncommon variant with features of poor prognosis and dedifferentiation. Disclosures: No relevant conflicts of interest to declare.

scholarly journals Oxaliplatin-Induced Pulmonary Toxicity in Gastrointestinal Malignancies: Two Case Reports and Review of the Literature

2015 ◽  
Vol 2015 ◽  
pp. 1-5 ◽  
Author(s):  
Mor Moskovitz ◽  
Mira Wollner ◽  
Nissim Haim
Keyword(s):  
Side Effect ◽  
Pulmonary Toxicity ◽  
Case Reports ◽  
Sensory Neuropathy ◽  
Common Side Effect ◽  
Hematological Toxicity ◽  
Review Of The Literature ◽  
Peripheral Sensory Neuropathy ◽  
Gastrointestinal Malignancies ◽  
Peripheral Sensory

Oxaliplatin is a common chemotherapy drug, used mainly for colon and gastric cancer. Most common side effects are peripheral sensory neuropathy, hematological toxicity, and allergic reactions. A less common side effect is pulmonary toxicity, characterized mainly by interstitial pneumonitis. The incidence of this side effect is unknown, but the toxicity can be fatal. Twenty-six cases of pulmonary toxicity have been described in the literature, seven in the setting of adjuvant treatment. We describe two fatal cases of pulmonary injury related to oxaliplatin and a review of the literature.

Abstract 14877: A Never Ending Tale of Pericarditis

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Michel Ibrahim ◽  
Michael Fattouh ◽  
Omar Siddiqi ◽  
Alice K Jacobs
Keyword(s):  
Decision Making ◽  
Case Reports ◽  
Systolic Dysfunction ◽  
Management Strategies ◽  
Interdisciplinary Team ◽  
Pericardial Tamponade ◽  
Prior History ◽  
Acute Pericarditis ◽  
History Of

Background: The evidence on recurrent pregnancy-related pericarditis is limited, and management strategies are based mainly on case reports and expert opinion. Case: A 25-year-old G2P1, 28-week pregnant female, with a history of presumed viral pericarditis complicated by pericardial tamponade and recurrent colchicine resistant pericarditis which was successfully treated with a prolonged steroid taper in the postpartum period, now 1 year in remission presents with shortness of breath and pleuritic chest pain with elevated inflammatory consistent with prior presentation of myo-pericarditis. A trans-thoracic echocardiogram (TTE) revealed a mild pericardial effusion without evidence of systolic dysfunction, and pericardial tamponade. Decision-Making: Given prior history of pregnancy related colchicine resistant pericarditis which was complicated by pericardial tamponade around her prior delivery time, it was decided by an interdisciplinary team involving rheumatology, cardiology and obstetrics, to initiate prednisone 10 mg daily. Symptoms subsequently subsided with a down trend of cardiac and inflammatory biomarkers. Daily 10 mg prednisone was to be continued up through delivery but within 2 months she presented yet again with a similar clinical picture and was diagnosed with recurrence of disease. Her prednisone was increased to 20 mg daily with symptom resolution. Two weeks later, she went into labor and received stress dose steroids. She had a normal spontaneous vaginal delivery without any complications. She continued the same dose of 20 mg of prednisone until her follow-up with rheumatology when the decision was made to initiate azathioprine and slowly titrate off the steroids. Conclusion: The case highlights not only the rare association between pregnancy and recurrent pericarditis but also the complexity of its management. The case of our patient underscores the importance of family planning, shared-decision making, and management by an interdisciplinary team comprised of rheumatology, obstetrics/gynecology, and cardiology. There are currently no known well controlled trials of therapy for pregnancy related idiopathic recurrent acute pericarditis.

Features and Risk Factors of Peripheral Neuropathy during Treatment of Advanced Multiple Myeloma with Bortezomib.

Blood ◽  
2006 ◽  
Vol 108 (11) ◽  
pp. 5098-5098
Author(s):  
Jean El-Cheikh ◽  
Anne Marie Stoppa ◽  
Segolene Duran ◽  
Reda Bouabdallah ◽  
Norbert Vey ◽  
...  
Keyword(s):  
Multiple Myeloma ◽  
Peripheral Neuropathy ◽  
Dose Reduction ◽  
Median Time ◽  
Median Duration ◽  
Univariate Analysis ◽  
Autologous Transplantation ◽  
Prior History ◽  
History Of

Abstract Bortezomib has demonstrated activity and safety in heavily pretreated patients with relapsed and/or refractory multiple myeloma (MM). Peripheral neuropathy (PN) is among the most frequent adverse events reported with bortezomib, requiring dose-adjustment and careful patient-clinical monitoring. The aim of this retrospective single centre study was to determine the frequency, characteristics, and reversibility of PN from bortezomib treatment of 100 consecutive advanced MM patients treated with bortezomib 1.0 or 1.3 mg/m2 IV bolus on days 1, 4, 8, and 11, every 21 days. PN was evaluated by investigator neurological examination at baseline, during the study, and at last follow-up. Patients characteristics at baseline prior to bortezomib initiation were as follow: median age: 60 (range, 27–77), prior history of diabetes: n=8 (8%), prior autologous transplantation: n=76 (76%), prior treatment with thalidomide: n=75 (75%) with a median dose of 200 (range, 50–600) mg for a median duration of 8 (range, 1–61) months. Median duration between thalidomide discontinuation and bortezomib initiation was 5 (range, 0–43) months. Before treatment with bortezomib, 48 patients (48%) already had some form of PN [grade 1, n=27 (56%); grade 2, n=16 (33%); grade 3, n=5 (11%)]. With a median follow-up of 8 (range, 0.1–32) months from bortezomib initiation, patients from this series received a median of 4 (range, 1–12) cycles of bortezomib. Bortezomib-related emergent PN was observed in 38 patients (38%; 95%CI, 28–47%), with grade 1, 2, 3, and 4 PN occurring in 17 (45%), 15 (39%), 5 (13%) and 1 (3%) patients respectively. Median time to onset of bortezomib-related PN was 53 (range, 11–182) days after bortezomib initiation. In most cases (n=30; 79%), patients had sensory symptoms, while 8 patients (21%) experienced both sensory and motor symptoms. Bortezomib-related PN led to dose reduction or discontinuation in 18 patients. Of the 38 patients with bortezomib-related PN, resolution to baseline or improvement occurred in 20 (53%) patients, at a median time of 3 (range, 1–8) months. In univariate analysis, comparing patients with and without bortezomib-related PN, prior history of treatment with thalidomide (P=0.009), patient baseline grade of PN at bortezomib initiation (P=0.04), number of bortezomib cycles administered (P=0.0005), and cumulative dose (mg) of bortezomib received by patients (P=0.001), were found to be significantly associated with the risk of emergence of bortezomib-related PN. In multivariate analysis, the total number of cycles of bortezomib (less or more than 4 cycles), and a prior history of treatment with thalidomide were the strongest parameters significantly associated with an increased incidence of bortezomib-related PN (P=0.03; OR=2.6; 95%CI, 1.1–6.1 and P=0.02; OR=3.9; 95%CI, 1.2–12.6 respectively). In all, we conclude that, though relatively frequent, bortezomib-associated PN seemed reversible in a majority of patients and manageable after dose reduction or discontinuation. However, the finding that the development of bortezomib-related PN seems to be dependent of the patient history of prior neurotoxic therapy (mainly thalidomide), raises the question of the optimal sequence and schedule of administration of these anti-MM effective drugs as single agents, but also in combination.

A rivastigmine-precipitated manic episode in a patient with Alzheimer-type dementia

2012 ◽  
Vol 24 (10) ◽  
pp. 1697-1699 ◽  
Author(s):  
Wei-Shih Tseng ◽  
Nian-Sheng Tzeng
Keyword(s):  
Cholinesterase Inhibitors ◽  
Case Reports ◽  
Manic Episode ◽  
First Episode ◽  
Prior History ◽  
Alzheimer Type ◽  
Geriatric Population ◽  
Alzheimer Type Dementia ◽  
History Of ◽  
Secondary Mania

ABSTRACTThe occurrence of mania in the geriatric population is rare. Furthermore, there were only six case reports of elderly patients with secondary mania resulting from treatment with cholinesterase inhibitors. In all cases, patients had a prior psychiatric history. We report the case of an elderly patient with no prior history of psychiatric or other organic disorders who experienced first episode mania following treatment with rivastigmine. We discuss the possible mechanism of mania in this patient.

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