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Chalazia Development in Multiple Myeloma: A New Complication Associated with Bortezomib Therapy.

Yun C, Mukhi N, Kremer V, Shinder R, Verma V, Olcay B - Hematol Rep (2015)

Bottom Line: Multiple myeloma (MM) is a neoplasm of plasma cells within the bone marrow.A major impact on improving survival in MM has been the use of the boronic acid-derived proteasome inhibitor bortezomib, a first-in-class selective inhibitor of the 26S proteasome.Ocular side effects of bortezomib are rare.

View Article: PubMed Central - PubMed

Affiliation: Division of Hematology/Oncology , New York, NY, USA.

ABSTRACT
Multiple myeloma (MM) is a neoplasm of plasma cells within the bone marrow. A major impact on improving survival in MM has been the use of the boronic acid-derived proteasome inhibitor bortezomib, a first-in-class selective inhibitor of the 26S proteasome. Ocular side effects of bortezomib are rare. In this report, we present 2 patients with active MM in whom persistent chalazia became a therapy-interfering complication of treatment with bortezomib. Both patients had relapsed ISS III B kappa light chain myeloma, and they were responding to treatment with bortezomib until chalazia - which caused intolerable discomfort - started. In both patients discontinuation of bortezomib was necessary for chalazia to heal, and restarting of bortezomib was associated with relapse of chalazia.

No MeSH data available.


Related in: MedlinePlus

Patients’ upper eyelid lesions (A, B) and their improvement (C)
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fig001: Patients’ upper eyelid lesions (A, B) and their improvement (C)

Mentions: A 56 year old African-American female presented in 2006 with a 2 month history of worsening pain in rib cage and upper back. Physical exam was positive for point tenderness on multiple ribs and in thoracic spine. Complete blood count displayed: white blood count (WBC) 2990/mm3 with normal differential, hemoglobin (HB) 12.5 g/dL, platelet count 144,000/mm3; blood urea nitrogen (BUN) 50 g/dL, serum creatinine (Cr) 5.6 mg/dL, calcium 10.2 mg/dL, b2 microglobulin 16.5 mg/L and albumin 3.0 mg/dL. Liver function tests and serum protein electrophoresis were within normal limits. 24 hours urine protein electrophoresis displayed 2 g/L b-band. Skeletal X-ray survey showed disseminated lytic lesions. Bone marrow biopsy showed 6% monotypic plasma cells expressing κ light chains with normal cytogenetics. She was diagnosed with ISS Stage IIIB κ light chain myeloma was treated with upfront thalidomide 200 mg per os/day, dexamethasone 40 mg per os /week and Doxil 20 mg/m2 intravenously, with the intention to receive HDCT and ASCT. After 4 cycles (120 days) she achieved a very good partial remission (VGPR) with disappearance of the κ-light chains in the urine by immunofixation and resolution of 50% of the skeletal lytic lesions. She refused further therapy. However, returned to clinic on January of 2014 with a painful new rib lytic lesion detected on X-ray. Serum free κ light chains were 3020 mg/L and free λ light chains were 8.30 mg/L with a κ/λ ratio of 364. Bortezomib 1.3 mg/m2 sc and dexamethasone 40 mg po weekly was started. After 2 cycles (36 days) she developed bilateral subcutaneous mildly tender, extremely itchy upper eyelid lesions 7×10 mm that were diagnosed by ophthalmology as acute chalazia (Figure 1A,B) with coexisting mild conjunctivitis. Bortezomib was held, and the eye the lesions were managed conservatively with warm saline compresses applied TID at home by the patient. Bortezomib was restarted after a 2 week lapse, as she had symptomatic relief from ophthalmic treatment, chalazia decreased in size by >75% and conjunctivitis cleared. After the second week of bortezomib reinitiation additional multiple bilateral chalazia with painful conjunctivitis developed, at which point bortezomib was held another week and she ophthalmology prescribed topical tobramycin/dexamethasone eye drops applied TID during the day and in ophthalmic ointment form to be applied at night, along with continued use of warm compresses. This treatment led to improvement of her eye lesions while on bortezomib (Figure 1C). Patient currently continues to receive bortezomib 1.3 mg/m2 weekly with dexamethasone 20 mg/week and uses topical tobramycin/dexamethasone eye drops. Her most recent serum free κ light chains are 2284 mg/L and free lambda (λ) light chains are 13.20 mg/L with a κ/λ ratio of 173. Bone marrow showed 30% cellularity with 10-15% κ-restricted plasma cells. FISH showed gain of 1q21; monosomy 13; gain of 9, 15 and gain of FGFR3/4p, CCND1/11q, IGH14q sequences; and loss of MAF/16q, indicating that biology of her disease had changed for the worse since 2006. She is willing to have her stem cells collected for possible ASCT/HDCT.


Chalazia Development in Multiple Myeloma: A New Complication Associated with Bortezomib Therapy.

Yun C, Mukhi N, Kremer V, Shinder R, Verma V, Olcay B - Hematol Rep (2015)

Patients’ upper eyelid lesions (A, B) and their improvement (C)
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4508549&req=5

fig001: Patients’ upper eyelid lesions (A, B) and their improvement (C)
Mentions: A 56 year old African-American female presented in 2006 with a 2 month history of worsening pain in rib cage and upper back. Physical exam was positive for point tenderness on multiple ribs and in thoracic spine. Complete blood count displayed: white blood count (WBC) 2990/mm3 with normal differential, hemoglobin (HB) 12.5 g/dL, platelet count 144,000/mm3; blood urea nitrogen (BUN) 50 g/dL, serum creatinine (Cr) 5.6 mg/dL, calcium 10.2 mg/dL, b2 microglobulin 16.5 mg/L and albumin 3.0 mg/dL. Liver function tests and serum protein electrophoresis were within normal limits. 24 hours urine protein electrophoresis displayed 2 g/L b-band. Skeletal X-ray survey showed disseminated lytic lesions. Bone marrow biopsy showed 6% monotypic plasma cells expressing κ light chains with normal cytogenetics. She was diagnosed with ISS Stage IIIB κ light chain myeloma was treated with upfront thalidomide 200 mg per os/day, dexamethasone 40 mg per os /week and Doxil 20 mg/m2 intravenously, with the intention to receive HDCT and ASCT. After 4 cycles (120 days) she achieved a very good partial remission (VGPR) with disappearance of the κ-light chains in the urine by immunofixation and resolution of 50% of the skeletal lytic lesions. She refused further therapy. However, returned to clinic on January of 2014 with a painful new rib lytic lesion detected on X-ray. Serum free κ light chains were 3020 mg/L and free λ light chains were 8.30 mg/L with a κ/λ ratio of 364. Bortezomib 1.3 mg/m2 sc and dexamethasone 40 mg po weekly was started. After 2 cycles (36 days) she developed bilateral subcutaneous mildly tender, extremely itchy upper eyelid lesions 7×10 mm that were diagnosed by ophthalmology as acute chalazia (Figure 1A,B) with coexisting mild conjunctivitis. Bortezomib was held, and the eye the lesions were managed conservatively with warm saline compresses applied TID at home by the patient. Bortezomib was restarted after a 2 week lapse, as she had symptomatic relief from ophthalmic treatment, chalazia decreased in size by >75% and conjunctivitis cleared. After the second week of bortezomib reinitiation additional multiple bilateral chalazia with painful conjunctivitis developed, at which point bortezomib was held another week and she ophthalmology prescribed topical tobramycin/dexamethasone eye drops applied TID during the day and in ophthalmic ointment form to be applied at night, along with continued use of warm compresses. This treatment led to improvement of her eye lesions while on bortezomib (Figure 1C). Patient currently continues to receive bortezomib 1.3 mg/m2 weekly with dexamethasone 20 mg/week and uses topical tobramycin/dexamethasone eye drops. Her most recent serum free κ light chains are 2284 mg/L and free lambda (λ) light chains are 13.20 mg/L with a κ/λ ratio of 173. Bone marrow showed 30% cellularity with 10-15% κ-restricted plasma cells. FISH showed gain of 1q21; monosomy 13; gain of 9, 15 and gain of FGFR3/4p, CCND1/11q, IGH14q sequences; and loss of MAF/16q, indicating that biology of her disease had changed for the worse since 2006. She is willing to have her stem cells collected for possible ASCT/HDCT.

Bottom Line: Multiple myeloma (MM) is a neoplasm of plasma cells within the bone marrow.A major impact on improving survival in MM has been the use of the boronic acid-derived proteasome inhibitor bortezomib, a first-in-class selective inhibitor of the 26S proteasome.Ocular side effects of bortezomib are rare.

View Article: PubMed Central - PubMed

Affiliation: Division of Hematology/Oncology , New York, NY, USA.

ABSTRACT
Multiple myeloma (MM) is a neoplasm of plasma cells within the bone marrow. A major impact on improving survival in MM has been the use of the boronic acid-derived proteasome inhibitor bortezomib, a first-in-class selective inhibitor of the 26S proteasome. Ocular side effects of bortezomib are rare. In this report, we present 2 patients with active MM in whom persistent chalazia became a therapy-interfering complication of treatment with bortezomib. Both patients had relapsed ISS III B kappa light chain myeloma, and they were responding to treatment with bortezomib until chalazia - which caused intolerable discomfort - started. In both patients discontinuation of bortezomib was necessary for chalazia to heal, and restarting of bortezomib was associated with relapse of chalazia.

No MeSH data available.


Related in: MedlinePlus