Project Title

VITAMIN B12 DEFICIENCY ANEMIA-ASSOCIATED MALIGNANCY ACCELERATED BY SUPPLEMENTATION

Authors' Affiliations

Dr. Neethu Nair, Dr. Christine Moore, Dr. Venkata Sri Harsha Vedantam, Dr. Diana Gorman-Nunley Department Of Internal Medicine, Quillen College of Medicine,East Tennessee State University, Johnson City,TN

Location

Clinch Mtn. Room 215

Start Date

4-5-2018 8:00 AM

End Date

4-5-2018 12:00 PM

Poster Number

158

Name of Project's Faculty Sponsor

Diana Gorman-Nunley

Faculty Sponsor's Department

Internal medicine

Type

Poster: Competitive

Classification of First Author

Medical Resident or Clinical Fellow

Project's Category

Biomedical Case Study

Abstract Text

Vitamin B12 and folate are necessary for bone marrow progenitor growth and division. Deficiencies are common in lymphoproliferative disorders due to increased demands of rapidly growing malignant cells. Isolated vitamin B12 deficiency is seen in 13% of these patients and may be their only manifestation. We present the case of vitamin B12 deficiency anemia due to an underlying malignancy that was discovered following supplementation.

A 77-year-old nonsmoker female with chronic kidney disease and hypothyroidism presented to her internist with dyspnea, tachycardia and unintentional 7-pound weight loss. Age-appropriate cancer screenings were up-to-date. Physical exam was notable for an overweight female with tachycardia and trace ankle edema bilaterally. Electrocardiogram demonstrated sinus tachycardia. Labs were remarkable for hemoglobin 10.3 mg/dL (12.1 mg/dL one year ago) and serum B12/mL. She was started on intramuscular vitamin B12 supplementation. At her one-month follow-up, she reported debilitating gastrointestinal distress, rash, and fatigue lasting 5-6 days with every vitamin B12 injection. Physical exam was notable for 20-pound weight loss. Labs revealed hemoglobin 9.9 mg/dL despite serum B12 750 pg/mL and worsening kidney function with marked proteinuria. Additional work-up by primary team and subsequent Hematology & Oncology referral demonstrated elevated M-spike on urine protein electrophoresis and abnormal bone marrow biopsy suspicious for lymphoid malignancy. CT abdomen and whole body PET scan revealed increased uptake in the T12 vertebrae and multiple nodal basins consistent with stage IV lymphoma. Biopsy of vertebral body confirmed diffuse large B-cell lymphoma. The patient received one cycle of chemotherapy with R-CHOP (rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone). Her course was complicated by pathologic hip fracture requiring hospitalization and surgical repair. The patient died following cardiac arrest in the setting of septic shock from sigmoid colon perforation 7 months from initial presentation.

Vitamin B12 and folate play critical roles in nucleic acid synthesis for bone marrow progenitors. Vitamin B12 deficiency arrests cell growth and division, leading to macrocytic anemia and various neuropsychiatric manifestations. It is a common diagnosis with numerous causes: autoantibodies to digestive proteins, poor dietary intake, small bowel malabsorption, etc. Diagnose with low hemoglobin (/dL or 13 mg/dL in non-pregnant women or men, respectively) and mean corpuscular volume >100 fL plus low serum B12 or elevated homocysteine and methyl-malonic acid levels. Replacement is given orally or intramuscularly. Vitamin B12 and folate deficiencies are found in lymphoproliferative disorders due to increased demands of rapidly growing malignant cells. Isolated vitamin B12 deficiency is seen in 13% of patients and may be the only clue. Replacement will not resolve their anemia. Physicians should monitor patients receiving supplementation. If anemia fails to improve or patients experience systemic symptoms, further investigation for lymphoid malignancies is warranted. This patient had dramatic deterioration with acceleration of underlying malignancy following vitamin B12 replacement. We believe supplementation enabled malignant lymphoid precursors to resume cell cycle growth and division. Only one report of vitamin B12 supplementation associated with unmasking a lymphoid malignancy exists in literature. Further research is needed to support whether supplementation can accelerate lymphoid malignancies.

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Apr 5th, 8:00 AM Apr 5th, 12:00 PM

VITAMIN B12 DEFICIENCY ANEMIA-ASSOCIATED MALIGNANCY ACCELERATED BY SUPPLEMENTATION

Clinch Mtn. Room 215

Vitamin B12 and folate are necessary for bone marrow progenitor growth and division. Deficiencies are common in lymphoproliferative disorders due to increased demands of rapidly growing malignant cells. Isolated vitamin B12 deficiency is seen in 13% of these patients and may be their only manifestation. We present the case of vitamin B12 deficiency anemia due to an underlying malignancy that was discovered following supplementation.

A 77-year-old nonsmoker female with chronic kidney disease and hypothyroidism presented to her internist with dyspnea, tachycardia and unintentional 7-pound weight loss. Age-appropriate cancer screenings were up-to-date. Physical exam was notable for an overweight female with tachycardia and trace ankle edema bilaterally. Electrocardiogram demonstrated sinus tachycardia. Labs were remarkable for hemoglobin 10.3 mg/dL (12.1 mg/dL one year ago) and serum B12/mL. She was started on intramuscular vitamin B12 supplementation. At her one-month follow-up, she reported debilitating gastrointestinal distress, rash, and fatigue lasting 5-6 days with every vitamin B12 injection. Physical exam was notable for 20-pound weight loss. Labs revealed hemoglobin 9.9 mg/dL despite serum B12 750 pg/mL and worsening kidney function with marked proteinuria. Additional work-up by primary team and subsequent Hematology & Oncology referral demonstrated elevated M-spike on urine protein electrophoresis and abnormal bone marrow biopsy suspicious for lymphoid malignancy. CT abdomen and whole body PET scan revealed increased uptake in the T12 vertebrae and multiple nodal basins consistent with stage IV lymphoma. Biopsy of vertebral body confirmed diffuse large B-cell lymphoma. The patient received one cycle of chemotherapy with R-CHOP (rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone). Her course was complicated by pathologic hip fracture requiring hospitalization and surgical repair. The patient died following cardiac arrest in the setting of septic shock from sigmoid colon perforation 7 months from initial presentation.

Vitamin B12 and folate play critical roles in nucleic acid synthesis for bone marrow progenitors. Vitamin B12 deficiency arrests cell growth and division, leading to macrocytic anemia and various neuropsychiatric manifestations. It is a common diagnosis with numerous causes: autoantibodies to digestive proteins, poor dietary intake, small bowel malabsorption, etc. Diagnose with low hemoglobin (/dL or 13 mg/dL in non-pregnant women or men, respectively) and mean corpuscular volume >100 fL plus low serum B12 or elevated homocysteine and methyl-malonic acid levels. Replacement is given orally or intramuscularly. Vitamin B12 and folate deficiencies are found in lymphoproliferative disorders due to increased demands of rapidly growing malignant cells. Isolated vitamin B12 deficiency is seen in 13% of patients and may be the only clue. Replacement will not resolve their anemia. Physicians should monitor patients receiving supplementation. If anemia fails to improve or patients experience systemic symptoms, further investigation for lymphoid malignancies is warranted. This patient had dramatic deterioration with acceleration of underlying malignancy following vitamin B12 replacement. We believe supplementation enabled malignant lymphoid precursors to resume cell cycle growth and division. Only one report of vitamin B12 supplementation associated with unmasking a lymphoid malignancy exists in literature. Further research is needed to support whether supplementation can accelerate lymphoid malignancies.