Hepatic failure caused by plasma cell infiltration in multiple myeloma

Rahhal, Fadi; Schade, Robert R.; Nayak, Asha; Coleman, Teresa

doi:10.3748/wjg.15.2038

Cited by 23 publications

(28 citation statements)

References 17 publications

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“…Particularly cell adhesion molecules CD44 and CD56 which mediate myeloma cell adhesion to bone marrow stroma. Galani et al, theorized that cell adhesion molecule expression changes during the course of disease [21]. In 2012, Usmani et al published that the incidence of extramedullary myeloma was increased in patients treated with novel agents at their Multiple Myeloma Institute in Arkansas [22].…”

Section: Resultsmentioning

confidence: 99%

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Extramedullary Multiple Myeloma Mimicking Liver Metastases during Carfilzomib Treatment

Mensah¹

2017

J Blood Disord

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Section: Resultsmentioning

confidence: 99%

“…It's postulated that cell adhesion molecule expression is responsible for the spread of multiple myeloma cells outside of the bone marrow [21]. Particularly cell adhesion molecules CD44 and CD56 which mediate myeloma cell adhesion to bone marrow stroma.…”

Section: Resultsmentioning

confidence: 99%

Extramedullary Multiple Myeloma Mimicking Liver Metastases during Carfilzomib Treatment

Mensah¹

2017

J Blood Disord

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“…Laboratory investigations revealed Hb-8.8 g/dL, white cell counts-570 9 10 9 /l, differential counts-68 % polymorphs, 22 % lymphocytes, 8 % monocytes and 2 % eosinophils, platelets-533 9 10 9 /l, sedimentation rate-45 mm/hour, total bilirubin-15.50 mg/dl, direct fraction-12. [2]. Liver involvement in myeloma can take multiple forms including extramedullary plasmacytoma (space occupying lesion), light chain deposition, amyloidosis or diffuse plasma cell infiltration.…”

mentioning

confidence: 99%

“…Liver involvement in myeloma can take multiple forms including extramedullary plasmacytoma (space occupying lesion), light chain deposition, amyloidosis or diffuse plasma cell infiltration. Clinical manifestations vary from asymptomatic elevation of ALP with normal or slightly elevated aminotransferase levels to liver failure secondary to massive plasma cell or amyloid infiltration [2,3]. Treatment of myeloma is plagued by DILI as vinca alkaloids and anthracyclins are hepatotoxic and thalidomide may also be hepatotoxic.…”

mentioning

confidence: 99%

“…Steroids and bortezomib were considered hepato-safe in myeloma till recently when concerns were raised regarding bortezomib induced hepatotoxicity. [2,4] Thrombocytopenia, peripheral neuropathy and gastrointestinal side effects are the most commonly reported adverse events with bortezomib [5]. Since its first recognition in 2005 by Rosinol et al [6], few cases of bortezomib induced hepatitis have been described thereafter.…”

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confidence: 99%

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Cholestasis in a Patient of Multiple Myeloma: A Rare Occurrence of Bortezomib Induced Liver Injury

Jain

Malhotra

Suri

et al. 2016

Indian J Hematol Blood Transfus

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Drug induced liver injury (DILI) is a common cause of jaundice (2-10 %) in hospitalized settings. Diagnosing DILI clinically is a dogmatic task as DILI can mimic almost any cause of acute or chronic hepatitis. Lack of specific clinical, biochemical or imaging findings and concomitant systemic illness makes DILI a diagnosis of exclusion, recognition of which is extremely important to prevent long term hepatic injury.[1] We report a 54 yearsold non-alcoholic man who initially presented to our hematology clinic with complaints of backache of 3 months duration. Investigations revealed anemia (Hb: 8 g/dl), renal failure (Creatinine: 3.2 mg/dl), hypercalcemia (calcium: 12.4 mg/dl), sedimentation rate of 98 mm/ h and punched out Lytic lesions in skull, pelvis and vertebrae. Bone marrow aspirate revealed 32 % plasma cells. Serum protein electrophoresis (SPEP) with immune-fixation identified monoclonal (M) band (4.2 g/l, IgG Kappa), thereby confirming a diagnosis of Multiple myeloma ISS-II (b2 microglobulin-4 mg/dl). Urine electrophoresis and Bence jones proteins were negative. Liver function tests (LFT) and viral serologies for hepatitis B, hepatitis C and HIV were normal. Hypercalcemia and renal dysfunction were managed with saline hydration and bisphosphonates followed by a combination of oral Cyclophosphamide (300 mg/m 2 ) and dexamethasone (40 mg) administered weekly and bortezomib (1.3 mg/m 2 ) on day 1, 4, 8 and 11 in a 4 weekly schedule (CyBorD). Cotrimoxazole and Acyclovir were used as prophylaxis for Pneumocystis jeroveci and herpes zoster respectively. Serum calcium and Creatinine levels normalized following the first cycle. Patient presented currently with jaundice and pruritus 2 days after receiving second dose of bortezomib during second cycle of CyBorD. He denied any fever, abdominal pain and herbal drug intake. Patient was conscious, oriented to time, place and person with blood pressure-120/ 72 mm hg, pulse rate-72/min. General examination revealed marked icterus without any features of hepatic encephalopathy. Abdomen examination revealed hepatomegaly (4 cm) in the absence of free fluid or splenomegaly. Rest of the systemic examination was unremarkable. Laboratory investigations revealed Hb-8.8 g/dL, white cell counts-570 9 10 9 /l, differential counts-68 % polymorphs, 22 % lymphocytes, 8 % monocytes and 2 % eosinophils, platelets-533 9 10 9 /l, sedimentation rate-45 mm/hour, total bilirubin-15.50 mg/dl, direct fraction-12

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Efficacy and tolerability of the histone deacetylase inhibitor panobinostat in clinical practice

Baertsch

Hillengaß

Blocka

et al. 2017

Hematological Oncology

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The histone deacetylase inhibitor panobinostat has shown efficacy in phase-II and phase-III trials for multiple myeloma and has recently received market approval in combination with bortezomib and dexamethasone. Here, we retrospectively report our single center experience with panobinostat/bortezomib/dexamethasone (FVD) in a heavily pretreated patient population (n = 24) with a high degree of refractoriness to proteasome inhibitors (PI) and immunomodulatory drugs (IMiD). Median age was 67 years (range 49-87) and the median number of prior therapies was 5 (range 2-17). Fourteen patients (58%) had high-risk cytogenetic aberrations. Thirteen (54%) and 21 (88%) patients were refractory to PIs and IMiDs, respectively. Twelve patients (50%) were refractory to bortezomib and 7 (29%) to carfilzomib; 6 patients (25%) were refractory to both bortezomib and carfilzomib. In 21 patients evaluable for response, overall response rate (ORR; ≥PR) was 33% (7/21) and 81% (17/21) achieved at least stable disease. Median progression-free survival (PFS) and overall survival were 3.5 and 9.8 months, respectively. Significant differences between bortezomib-sensitive and -refractory patients were observed. In bortezomib-sensitive patients, median PFS was 6.3 months compared to 2.3 months in bortezomib-refractory patients (P < .001). Median overall survival was not reached vs 4.8 months (P = .046) in bortezomib-sensitive and bortezomib-refractory patients, respectively. The only patient refractory to carfilzomib but sensitive to bortezomib achieved very good partial remission and PFS of 6.3 months, suggesting discrete mechanisms of resistance to different PIs. As expected, thrombocytopenia and fatigue/asthenia occurred in nearly all patients (96% and 83%, respectively). Diarrhea was observed in only 19% of patients which compares favorably with the high rates of diarrhea reported in the PANORAMA trials. With panobinostat dose reductions in 67% of patients, FVD was tolerated by the majority of patients. In conclusion, FVD showed efficacy in a heavily pretreated, high-risk multiple myeloma population with a high degree of patients refractory to novel agents including PIs.

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Hepatic failure caused by plasma cell infiltration in multiple myeloma

Cited by 23 publications

References 17 publications

Extramedullary Multiple Myeloma Mimicking Liver Metastases during Carfilzomib Treatment

Extramedullary Multiple Myeloma Mimicking Liver Metastases during Carfilzomib Treatment

Cholestasis in a Patient of Multiple Myeloma: A Rare Occurrence of Bortezomib Induced Liver Injury

Efficacy and tolerability of the histone deacetylase inhibitor panobinostat in clinical practice

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